Causes Of Dementia

Causes Of Dementia
The most common early and clinical symptoms of AD are disorientation, memory loss, language
loss and alteration, gradual decline in synaptic and neuronal loss, cognitive dysfunction, and
behavioral and physical disability (Snowden et al., 2011). With the rapid decline of AD conditions
and with the progress of dementia, it became a social aspect that affects the quality of life for
individuals and their interactions with social environment and occupational function. The functions
of the body are gradually lost resulting to death in the majority of cases. As reported, AD is
considered to be the sixth cause of death among devastating diseases in the US, and it is more
prevalent in women compared with men (rate/100 years, 2.50 women and 1.89 men) ... Show more
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The majority of described AD cases are due to SAD, which accounts for more than 90% of all cases.
Individuals who diagnosed with SAD, their symptoms commonly appear later after age 65. The
most common risk factors of SAD are believed to be multiple environmental risk factors, and
genetic pre–dispositions, which still remained elusive. One of the most known genetic risk factor
associated with SAD is apolipoprotein E4 (ApoE4 variant). It is believed that people carrying more
than one allele of ApoE4 are expected to be at higher risk of evolving AD later in their life
(Kivipelto et al., 2002). On the other hand, FAD accounts for only 5% of all cases compared with
SAD, and the symptoms of patients diagnosed with FAD usually appear before age 65 (Katayama et
al., 2001). The FAD form is commonly caused by inherited genetic factors. The most known and
possible factors of FAD type are attributed to be autosomal dominant mutations within three
important genes, which are genes encoding for amyloid precursor protein (APP) and presenilins 1
and 2 (PS1 and PS2), and both of which could result to increase the production of beta–amyloids
especially Aβ40 (Chadwick et al.,
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Essay on Alzheimer’s Disease
Alzheimer's Disease
Alzheimer's disease is a progressive condition where the neurons degenerate in the brain, while the
brain substance shrinks in volume. Alzheimer's is also the number one cause of dementia. When it
was first noticed, Alzheimer's was thought to be a pre–senile disease, but now it is known to be
responsible for seventy–five percent of the dementia cases in people over sixty–five years of age.
Alzheimer's disease usually causes several years of personal and intellectual decline until death.
Because there is an increasing number of elderly citizens in the United States, research into the
causes and possible cures for the disease is on the rise (1).
Several theories have been made concerning factors that may cause ... Show more content on
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Also, women are thought to be at a slightly higher risk than men (4).
The symptoms of the disease vary somewhat among individuals. However, there are three distinct
stages that a person suffering from Alzheimer's will experience. In the first stage, the patient
experiences some problems with memory loss and will often make lists or other aids to compensate
for this loss. The individual can begin to feel depressed or anxious because of the memory problems.
This stage often Goes unnoticed as symptoms of Alzheimer's (1).
The second stage is marked by the change from forgetfulness to severe memory loss. Long–aGo
events are often easier to recall than things that have happened within the last few days. For
example, one might remember childhood events but are unable to remember what they saw on
television last night or what they ate for breakfast. Disorientation in relation to time and place
occurs often, along with increased anxiety and recurring mood swings. The patient also experiences
dysphasia (inability in finding the right word to say), increased difficulty with math problems, and
loss of direction in familiar places. Personality changes will soon become noticeable when this
second stage is reached (1).
Finally, the third stage is marked by severe disorientation and confusion. Usually, the worst signs of
memory loss and disorientation occur at night. In this

The Chronic and Incurale Disease of Alzheimers Essay
What is Alzheimer's? It is a disease that affects the central nervous system, digestive system, the
neuromuscular system and is generally a disease that is chronic and incurable. 4.7 million people
greater than the age of 65 live with the disease each and every day, which is approximately one tenth
of the population for those over the age of 65. The most common questions are: what are the risk
factors, which vary from person to person, whether or not there are signs and symptoms and has
there been any testing and diagnosis on this disease. Well the first question usually asked by a vast
majority of those in the age range for such a disease is am I at risk for Alzheimer's. First you need to
know the risk factors involved when discussing ... Show more content on Helpwriting.net ...
There are so many signs and symptoms that correlate to the Alzheimer's disease, which include but
are not limited to: having a worsened ability to take in and remember new information, impairments
to reasoning and changes in personal behavior. Usually those who have Alzheimer's will have a hard
time taking in and remembering new information, meaning they will ask repetitive questions or start
conversations that were previously mentioned. A lot of times they will also misplace their personal
belongings and may even forget important appointments or their grand–children's baseball game.
When you have the Alzheimer's disease you may also find out that you get lost very easily on a
commonly traveled route. Finally the question everybody wants an answer to, are there tests that can
be done to find out if I have Alzheimer's and if I do have it is there a diagnosis of this disease?
Before go too far it should be known that there is not a single test for this disease and finding out if
you have it can be a very strenuous procedure. A doctor can do any number of things from taking
down the history of your family to arranging for brain scans to be done. The things that are most
commonly done however are: taking down family history, doing a physical examination and even
doing cognitive testing. Even in recent studies is has been found that using peanut butter can help
diagnose the Alzheimer's disease. The

Pathogenesis Lab Report
The pathogenesis of AD Is not yet fully understood. (H.Break and E.Break,1991)
The neuropathological hallmarks of AD are the presence of plaques and neurofibrillary tangles. (18
–20)
There are two main hypotheses explaining the pathogenesis of AD:
Amyloid cascade hypothesis
The β–amyloid plaques are an extracellular deposition of amyloid beta protein[21]. This protein is
derived from cleavage of the amyloid precursor protein (APP) by the β – and γ– secretase enzymes
[22] .
The accumulated amyloid bet npeptides can aggregatr into oligomer (24) And form plaques (16)
The Aβ deposition and diffused plaque formation lead to local microglial activation, cytokine
release, reactive astrocytosis and a multi–protein inflammatory response (Eikelenboom ... Show
more content on Helpwriting.net ...
the pathogenic mechanism of presenilin mutations which alters APP metabolism would be
responsible to elevate levels of Aβ peptides. (Bertram and Tanzi, 2008). followed by APOE, a major
genetic risk factor increase Aβ peptide aggregation and impair Aβ clearance in the brain for the
disorder in the typical late–onset period (Strittmatter and Roses, 1995). The genetic studies suggest
that neurodegenerative processes in AD are the consequences of an imbalance between Aβ peptide
production and clearance. However, physiological functions of APP are poorly understood (Yoshikai
et al., 1990; Ling et al., 2003; Muller and Zheng, 2012). The APP gene is located on chromosome 21
and those individuals suffer from Down's syndrome (trisomy 21) with an extra copy of this
chromosome develops an early–onset familial AD (EOFAD) (Yoshikai et al., 1990; Ling et al.,
2003). There are two proteolytic processing pathways of APP. In the non–amyloidogenic pathway,
APP cleaved by α and γ secretases resulted in the production of soluble form of APP (sAPPα). In
amyloidogenic pathway, APP cleaved by β–secretase generates membrane bound C–terminal
fragment (C99) which subsequently cleaved by γ secretase and produces Aβ peptide (Nunan and
Small, 2000; Selkoe and Schenk, 2003).
Tau hypothesis tau is an intracellular protein, necessary for the stabilization

Alzheimer's Disease Compromises Cognitive and Memory Skills
Alzheimer's disease is a progressive neurodegenerative disease of the brain wherein a person
afflicted with the said disease would have compromised cognition and memory skills, and eventual
deterioration of the skill to execute uncomplicated activities. According to experts, most individuals
do not manifest the symptoms for Alzheimer's disease until they are over the age of 60. This disease
affects more than 5.1 million Americans. Alzheimer's disease is named after Dr. Alois Alzheimer
who first discovered deviations from normal tissues of healthy individuals in the brain tissue of a
lady in 1906. The woman, who showed symptoms of erratic behavior, loss of memory, and problems
with communication, died of a then unfamiliar mental disorder. This led Dr. Alzheimer to investigate
the cause of her unusual death. He assessed the brain of the woman and found that there were many
anomalous masses (amyloid plaques) and intertwined bundles of fiber (neurofibrillary tangles).
Scientists today have pinpointed the qualities of Alzheimer's to be a) tangles in the brain
(neurofibrillary tangles), b) plaque in the brain (amyloid plaques), and c) loss of connections among
nerve cells. Experts know little about the true causes of AD (Alzheimer's disease), however they
have proposed the amyloid hypothesis to explain how the disease begins. In people afflicted with
AD, lethal transformations are happening in the brain. A buildup of amyloid plaque (β–amyloid
clumps), caused by the

Alzheimer 's Disease : A Complete Look At The Onset And...
Alzheimer 's Disease – A Complete Look at the Onset and Progression Alzheimer 's disease is a
condition that affects the cognitive status of many people around the world regardless of wealth,
ethnicity, intelligence or any other factor. A specific case study that demonstrates the destructive
nature of the disease can be seen in the case of Akram. Akram was an 80–year–old female with a
past medical history of hypertension, diverticulitis, transient ischemic attack (TIA), and diabetes.
She had a history of serious head injury at the age of 45 from an automobile accident, but she
recovered well after some time in the hospital. She could remember childhood friends and family
from 20+ years ago quite well. Her early symptoms were simple daily processes of life. She might
put food in the oven to cook, but fail to turn it on after doing all the prep work. She also began to
frequently misplace her keys and have trouble remembering where she put household items. She had
been a very intelligent person with a lot of energy and had previously been involved in many
volunteer projects she helped run. Her husband, mentioned that she had been having similar
difficulties over the past two years. Driving was a big issue as well; she felt she could recall how,
but still had trouble operating her vehicle. She also frequently got lost on routine trips, like to the
grocery store. Additionally, she would forget whether she had eaten and had several extra meals in a
day unless a helper or a

Alzheimer's Amyloid Hypothesis
Alzheimer's disease (AD) is an irreversible progressive neurological disorder affecting memory and
cognitive abilities (Qiu et al., 2009). As Estimated, patients diagnosed with AD may not survive the
disorder within three to nine years since their diagnosis. AD is the leading cause of dementia in
elderly patients, with increased incidence of prevalence with age. Every year, 1275 cases per
100,000 persons aged more than 65 are diagnosed, with a doubling in the incidence every five years
in patients older than 65 (Reitz et al., 2011). AD is a multifactorial disease with a unique pathogenic
protein aggregations, including accumulation of hyper–phosphorylated tau and the accumulation
and misfolding of Amyloid–β (Aβ) (Querfurth and LaFerla, 2010). ... Show more content on
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The spontaneous self–aggregation of Aβ into multiple coexisting physical forms, including
oligomers (two to six peptides), leads to their coalescence into intermediate assemblies. In addition
to this, β–amyloid can also grow into fibrils, which arrange themselves into β–pleated sheets to form
the insoluble fibers of advanced amyloid plaques. Soluble oligomers and intermediate amyloids are
the most neurotoxic forms of Aβ. In brain–slice preparations, synapses are toxified by dimers and
trimers of Aβ. However, the severity of the cognitive defect in Alzheimer's disease is in correlation
with the levels of oligomers in the brain, not the total burden of Aβ. Neuronal activation rapidly
increases Aβ secretion at the synapse, a process tied to the normal release of vesicles containing

Alzheimer's Disease Research Paper
Alzheimer's disease is a degenerative brain disease for which there is no recovery. Slowly, the
disease attacks nerve cells in all parts of the cortex, as well as some surrounding structures; thus
impairing the capacity of the person to govern emotions, recognize errors and patterns, coordinate
movement, and remember (Qué es la enfermedad de Alzheimer?, n.d., para. 1).
Until recently, two significant abnormalities were observed in the brain of patients affected by
Alzheimer's Disease: twisted nerve cell fibers, known as tangles neurofibrilares, and a protein called
beta amyloid (Qué es la enfermedad de Alzheimer?, n.d., para. 3).
The entangled fibers are remnants of damaged microtubules, the support structure that permits the
flow of nutrients ... Show more content on Helpwriting.net ...
These plaques are made out of nerve cells surrounded by dying neurons. The same beta amyloid is a
splice from a larger protein called amyloid precursor protein (Qué es la enfermedad de Alzheimer?,
n.d., para. 5).
Amyloid beta is also associated with reduced levels of the neurotransmitter protein acetylcholine.
An acetylcholine receptor is an integral membrane protein that forms part of essential processes like
memory and learning, which are progressively destroyed in patients with Alzheimer's disease (Qué
es la enfermedad de Alzheimer?, n.d., para. 6).
Researchers explain that apolipoprotein ApoE4, a subtype of ApoE, plays a role in the movement
and distribution of cholesterol to repair nerve cells during development and after injury. However,
patients without ApoE4 are at a low risk from developing Alzheimer's. Patients with one copy of the
gene have an increased chance of developing the disease than those with two copies of the gene
(only 25% of the population carries two copies of E4 gene). A recent study found that a specific
variation of the ApoE4 gene is associated with a higher risk of Alzheimer's disease, which may
explain why many people with ApoE4 do not show any signs of Alzheimer's (Qué es la enfermedad
de Alzheimer?, n.d., para.

Taking a Closer Look at Alzheimer's Disease Essay
What is Alzheimer's disease? Alzheimer's disease (AD) is the most common form of dementia
known today. The term "dementia" refers to a variety of conditions that arise from the loss of nerve
cell function and/or nerve cell death in the brain, including Alzheimer's disease, vascular dementia,
Parkinson's disease, Creutzfeldt–Jakob disease and other types of mixed dementia. Although all
types of dementia arise from neuronal damage and/or death, each form of dementia is associated
with distinct brain abnormalities and symptom patterns. Once a patient has been diagnosed with
dementia, a physician must conduct further tests in order to determine the exact form of dementia
that is present. Recent research indicates that many individuals, ... Show more content on
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Thus, the preclinical stage of AD currently cannot be diagnosed (cite). Mild Cognitive Impairment
(MCI) due to Alzheimer's disease This stage of AD is characterized by measurable changes in the
thinking abilities of the affected individual that are noticeable to the individual and those around
them. These changes are mild and do not affect the individual's ability to perform everyday tasks;
however, approximately 50% of individuals who seek medical attention for their MCI symptoms
will develop AD dementia in the next three to four years (cite). Dementia due to Alzheimer's disease
This stage of AD is characterized by memory, thinking and behavioral symptoms that dramatically
impair an individual ability to function normally. These symptoms are caused by AD related brain
changes and affect an individual's ability to perform everyday tasks (cite). Alzheimer's disease
Symptoms As with most diseases, the symptoms caused by AD vary for person to person. A
symptom seen in nearly every patient, however, is the gradually worsening ability to remember new
information (cite). Other common symptoms of AD include the following: Challenges in planning
and solving problems Difficulty completing familiar tasks at home, at work or at leisure Confusion
with time or place Trouble understanding visual images and spatial

Protein Atherosclerosis
Proteins are very important to our lives because they carry out a multitude of tasks in our body.
Proteins are linear chains of amino acids that adopt unique three–dimensional structures and are
packed into their particular native conformations. However, protein folding can also go wrong when
the inaccurate folding and clustering together of protein molecules, which are observed in numerous
human diseases such as: diabetes, atherosclerosis, cystic fibrosis, Creutzfeldt–Jakob, Huntington's,
Parkinson's, Alzheimer's disease and many other neurodegenerative as well as non–neurological
diseases. Since the amyloidosis is the largest group of protein misfolding disease, Fabrozop Chiti
and Christopher M. Dobson described clearly in the article "Protein ... Show more content on
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The misfolding proteins can lead to many different diseases for human bodies. So, it's important to
prevent or disrupt the pathways to a misfolded protein. To do so, we first need to understand the
function of protein folding, amyloid fibril as well as alpha helix, beta sheets, Aβ , and α–
Synuclein...how they affected the structures of each protein in certain diseases. Then, it would be a
good fundamental tool that may lead to the development for treating diseases. However, the
challenge in developing treatment to prevent the misfolding disorders is identifying the ideal stage at
which the protein misfolding and subsequent aggregation can be disrupted. For example,
Alzheimer's Disease, treatment methods for AD, we need to develop of protease inhibiters aimed at
stopping the Amyloid beta release and prevent the aggregation of

Neurodevelopmental and Neurocognitive Disorders Essay
Neurodevelopmental and Neurocognitive Disorders Until the twentieth century, little account was
taken of the special characteristics of psychopathology in children; maladaptive patterns considered
relatively specific to childhood, such as autism, received virtually no attention at all (Butcher &
Hooley, 2014). Today there is more attention paid to children with maladaptive behaviors and
scientific research has been done that demands more attention is paid to specific children's
behaviors, not the behaviors of adult as there are no fair comparisons that allow the diagnosis and
treatments of adult and children's behaviors to be equal. Neurodevelopment disorders in children
result in maladaptive behavior which appears in different life ... Show more content on
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N., Hooley, J. M., Mineka, 2014). The causal factors for ADHD in children have been much
debated. It still remains unclear to what extent the disorder results from environmental or biological
factors (Carr et al., 2006; Hinshaw et al., 2007), and recent researchers believe that biological
factors such as genetic inheritance will turn out to be important precursors to the development of
ADHD (Durston, 2003). But firm conclusions about any biological basis for ADHD must await
further research (Butcher & Hooley, 2014, p. 513). Treatment for ADHD that focuses on controlling
behavior with drugs has been promising. One particular treatment involved the effectiveness of
MTA fading procedures. According to the article, the findings suggest that in contrast to the
hypothesized deterioration in the relative benefit of behavioral modification between nine and 14
months (after completion of fading), the MTA behavior generalization and maintenance procedures
implemented through nine months apparently yield continuing improvement through 14 months,
with preservation of the relative position of behavior compared

Amyloid Β Precursor Protein Analysis
Amyloid–β Precursor Protein (APP) is a gene that provides instructions for making a protein called
amyloid precursor protein (Andrew, 2009). Amyloid precursor protein is found in several tissues and
organs including the brain and the spinal cord––in other words the central nervous system (Andrew,
2009). Some studies suggest that in the brain, APP help direct movement of nerve cells during early
development. For instance, APP may be involved in the regulation of synaptogenesis which is the
formation of synapses between neurons in the nervous system (Dawkins, 2014).
Additionally, APP is cut by enzymes that create smaller fragments that are often released outside the
cell. Some fragments that help play a role in AD are soluble amyloid precursor

Relationship Between Alzheimer's Disease And Down Syndrome
Relationship between Alzheimer Disease and Down syndrome Down Syndrome (DS) is a genetic
and developmental disorder that arises due to a certain biological defect during the fusion of
gametes to produce a new organism. The occurrence of his biological defects leads to an extra
partial or full copy of chromosome 21 in every cell in the individual's body. In other words, there are
more copies of chromosome 21 in every cells in that person's body instead of the normal pairs.
According to the article, more copies of chromosome 21 makes the genes in the body to be
unbalanced. Therefore, it causes an individual to have some delays and limitations in both physical
and intellectual developments. Alzheimer Disease (AD) is a very rapid and progressive

Alzheimer's Main Features
Examining these three main features of Alzheimer's disease
The brains of people with Alzheimer's disease have an abundance of two abnormal structures –
amyloid plaques and neurofibrillary tangles. These are made of misfolded proteins which can stick
together with other misfolded proteins to form insoluble aggregates. If these aggregates build up,
they can disrupt cellular communication and metabolism. The third main feature of Alzheimer's is
the loss of connections between cells leading to the ill–functioning and death of cells (Institute and
Aging, 2011).
Amyloid plaques
These plaques consisting largely of insoluble deposits of a toxic protein peptide called beta–amyloid
are found in the spaces between the nerve cells in the brain. Beta amyloid

Alzheimer's Disease Analysis
Alzheimer's disease is a degenerative, neurological disease that affects millions of people every
year. It is a specific type of dementia that affects both memory and cognitive functions. The cause of
the disease has been well studied along with many types of ion interactions that either lessen or
worsen symptoms. Currently there is no treatment for this disease, but many researchers are working
to find a cure.
Alzheimer's disease is categorized by slight impaired memory to severe cognitive loss (Mayeux,
2010). This can be seen by a loss in retaining new memories as well as a decrease in language,
reasoning and decision making (Mayeux, 2010). This disease is progressive and patients only get
worse with time and it finally ends in death with both mental and functional disabilities (Mayeux,
2010). This is seen mainly in people 65 and older and studies have shown that age and aging is the
highest risk factor for the developing the disease (Lundkvist, 2014).
The disease was discovered by a German neuropsychiatrist by the name of Alois Alzheimer. One of
his patients died after having ... Show more content on Helpwriting.net ...
Mohs, R. (2013). A Phase 3 Trial of Semagacestat for Treatment of Alzheimer's Disease. New
England Journal of Medicine, 369(4), 341–350.
Doody, R., Thomas, R., Farlow, M., Iwatsubo, T., Vellas, B., Joffe, S., ... Mohs, R. (2014). Phase 3
Trials of Solanezumab for Mild–to–Moderate Alzheimer's Disease. New England Journal of
Medicine, 370(4), 311–321.
Lambracht–Washington, D., & Rosenberg, R. (2013). Anti–amyloid–beta to tau–based
immunization: Developments in immunotherapy for Alzheimer's disease. ImmunoTargets and
Therapy, 2013(2), 105–114.
Lundkvist, J., Halldin, M., Sandin, J., Nordvall, G., Forsell, P., Svensson, S., ... Ekstrand, J. (2014).
The battle of Alzheimer's disease – the beginning of the future Unleashing the potential of academic
discoveries. Frontiers in Pharmacology,

The Cause Of Alzheimer's Disease
Unfortunately, I have seen first–hand the devastation Alzheimer's disease causes in someone's life.
My best friend's aunt, and my Great Aunt were both diagnosed with Alzheimer's when I was in
grade school. I didn't know anything about this disease, I only saw the progression and the clinical
manifestations of the disease. The second aspect of Alzheimer's that I didn't understand was how
doctors weren't able to cure this disease. Our textbook, McCance and Huether state, "Some diseases,
such as tuberculosis, identify a highly specific causative or etiologic agent or process. Others such
as Alzheimer's disease or arthritis, indicate changes of unclear cause. There is considerable need for
more research to validate mental health diagnosis" (XV). ... Show more content on Helpwriting.net
...
Patients effected with Alzheimer's experience deterioration in memory and cognition, along with
changes in their personality or behavior. These changes seen in Alzheimer's patients is believed to
occur due to neuronal death in the frontal lobe, and the hippocampus region of the temporal lobe.
However, the cause of neuronal death idiopathic. Currently doctors are using two different types of
treatments for patients with Alzheimer's. The first method of treatment targets the neurotransmitter
acetylcholine. Alzheimer's medication is targeting the depletion of cholinergic neurons in the basal
nucleus of Meynert. Cholinergic neurons are responsible for the production and release of the
neurotransmitter acetylcholine. Acetylcholinesterase inhibitors work to inhibit the enzyme
acetylcholinesterase which breaks down acetylcholine, in order to, increase the levels of
acetylcholine in the patient's brain infected with Alzheimer's (Wolfe 73). The second treatment
method targets a different neurotransmitter called glutamate. Wolfe also refers to the drug
memantine, "appears to slow cognitive decline in patients with moderate to severe Alzheimer's by
blocking excessive activity of a different neurotransmitter glutamate" (73). However, these two
treatment options are not effective long–term treatment options. For example, Acetylcholinesterase
inhibitors usually become ineffective within six months to a

The And Its Effects On Alzheimer 's Disease Essay
According to the Alzheimer's Association (AA), "more than 5 million Americans are living with
Alzheimer's disease" and this number is expected to triple by the year 2050. The AA website states
that Alzheimer's is the 6th leading cause of death in our country with 1 in 3 seniors dying from
Alzheimer's or other types of dementia. Because this disease effects so many people and because its
symptoms are so devastating, scientists are continually searching for the cause of Alzheimer's
disease (AD) in attempt to find treatment or a cure. Some scientists working in this field believe that
microbial infections may be underlying causes of the disease. There are many theories and studies
are being conducted to determine whether bacteria or viruses are playing some role in the
development of AD and other forms of dementia.
To understand how microbes may be involved in AD, we first must look at what physically happens
to the brain with this disease. There are two distinct aspects involved in Alzheimer's disease; beta–
amyloid plaques and tau tangles. Beta–amyloid plaques are formed when the amyloid precursor
protein (APP) which is present in the membrane of neurons (alz.org) is cleaved off by beta and
gamma–secretases (Chen et al., 2001). In a normal brain, alpha–secretase does the cleaving and the
body processes APP on its own (Chen, et al., 2001). In AD, the small pieces join to form beta–
amyloid plaques but as smaller individual pieces they can interfere with nerve signaling

Is The Amyloid Precursor Protein ( App ) Is Long...
Introduction:
The amyloid precursor protein (APP) is long associated with Alzheimer's disease (AD). It is a
single–pass transmembrane protein and is responsible for producing the neurotoxic Aβ plaque which
accumulates within the brain (O'Brien et al. 2011). This accumulation of Aβ is what characterises
AD. However, in spite of APP's detrimental role in the pathogenesis of AD, it has been recently
shown that APP can act as a neuroprotective molecule following traumatic brain injury (TBI).
Approximately 10 million people worldwide are affected by this disease every year and it is
projected that by 2020, TBI will surpass various diseases and become a major disease of burden
(Hyder et al. 2007). Thus, due to this increase in morbidity and burden, TBI is an urgent medical and
public problem.
APP's protective role in TBI is currently understood to be the product of ɑ–secretase pathway in
soluble amyloid precursor protein ɑ (sAPPɑ) (Corrigan et al. 2013). This pathway was discovered in
the previous year by the same researchers who used APP knockout mice. The knockout mice had
cognitive and motor functions that were severely compromised with impaired neuroreparative
abilities compared to its wild–type counterpart (Corrigan et al. 2012). When the knockout mice were
treated with sAPPɑ, however, their neuroreparative responses were restored.
Furthermore, the protective properties of APP are often correlated with its functions of synaptic
formation and repair and iron transport and

Transgenic Animal Model Essay
Alzheimer's disease is the leading form of dementia within the world's elderly population and given
that there exists an ever increasing percentage of the elderly population within society,
understanding this neurodegenerative disease has become more important than ever. It is a disease
associated with subcortical temporal lobe structures such as the Hippocampus, the Entorhinal
Cortex, the Amygdala, the Thalamus, among others. Clinically, those millions of individuals
suffering from the disease experience episodes of irreversible memory loss, changes in personality
and confusion (among a plethora of other symptoms). Physiologically, the disease is characterized
by the accumulation of insoluble amyloid beta plaques, derived from the amyloid precursor protein
(APP). Another characteristic marker for Alzheimer's dementia is the Hyper–phosphorylation of the
Tau protein which then aggregates to form insoluble neurofibrillary tangles (NFTs), that inhibit a
cell's ability to regulate the stabilization of the microtubule component tubulin. Transgenic animal
models have proven to be quite useful in terms of exploring the ways in which diseases manifest
themselves in humans. In regards to mouse models, their shorter lifespans along with their brain's
similarity to that of a human ... Show more content on Helpwriting.net ...
For this reason, an understanding of the cognitive impairments associated with the disease alongside
a characterization of the less prominent pathologies such as vascular pathologies should be studied.
Much is not yet known about vascular pathologies in the early stages of Alzheimer's disease;
however, if present in the early stages of the disease, greater amyloid beta build up would be found
in regions surrounding blood vessels in the 3xTg AD mice in comparison to a

Alzheimer 's Disease Of The Scientific World Essay
In 1906, Alzheimer's disease entered the scientific world. Till this day, it is one of the most studied
neurodegenerative diseases. Researchers have come a long way with scientific outcomes on the
disease, but unfortunately there is no official cure, or a concise reason on how this disease is
generated. The disease has been recognized to being genetic and affecting people in their later years,
roughly around their sixtieth year. Alzheimer's disease affects the person's memory, language,
judgment and even their daily tasks. While the disease continues to dramatically progress, it begins
to affect all regions of the brain, causing the person to lose almost all of their functions. When the
person has reached their final stage, they are no longer able to recognize themselves or their
surroundings and would need full time dependent care. According to the Alzheimer's Association
(alz.org, 2016), the person may have up to eight years max to live after diagnosis.
There are several methods in diagnosing Alzheimer's disease such as: asking the person about their
family medical history, conducting memory tests, carrying out standard medical tests (urine and
blood) and brain scans like CT's, MRI's and PET's (NIH.gov, 2016). The only way the disease can
be verified is after death, because brain tissue can then be studied for a complete diagnosis
(NIH.gov, 2016).
Researching Alzheimer's disease has been a continuous obstacle for all scientists. They have made
miraculous advances in their

The Correlation Between Down Syndrome And Alzheimer 's...
The Correlation between Down syndrome and Alzheimer's disease
Anna Lister
Biology Honors, P. 3
Mrs. Creech
25 November 2015
Introduction:
Alzheimer's disease (AD) is a disease that slowly and progressively causes memory impairment. It
will eventually inhibit abilities, such as language, planning, and perception. AD is prevalent in
individuals with Down syndrome (DS), a condition where those affected had acquired three
additional chromosome 21 before birth (emedicinehealth, 2014). Michael Rafii, director of the
Memory Disorders Clinic at UCSD, says that "people with Down syndrome represent the world 's
largest population of individuals predisposed to getting Alzheimer 's disease" (Hamilton, 2014).
There is no cure for either, and scientists are still lacking the knowledge of a complete story.
Beta Amyloid, Plaques, and the Destruction of Nerve Cells:
There is a large supply of amyloid plaques in the cells of people with Alzheimer's disease. Amyloid
plaques are clustered pieces of protein that build up between nerve cells. They speed up the
production of beta amyloid, which are polypeptides of about thirty–six to forty–three amino acids
long (emedicinehealth, 2014; Stanford Medicine, 2013). Amyloid precursor proteins (APP), when
split into specific pieces, are producers of beta amyloid. They are found in tissues and organs, such
as the brain. Amyloid precursor proteins pass through a fatty membrane on the outside of a cell. This
allows them to extend from the

Amyloid Precursor Protein Essay
Amyloid precursor protein (APP) has many functions and regulations. This protein is involved in
neural development. Many may know it for its involvement in the pathology of Alzheimer disease as
well as other neurodegenerative diseases. However, APP is a developmental gene. This gene
regulates neurons, their differentiation as well as migration. This gene is also involved in neurite
outgrowth and the regulation of synaptic function (1). Despite knowledge of these functions, many
functions of APP is still unclear (2).
Structure:
APP is a member of conserved type 1 membrane proteins which also includes amyloid precursor–
like proteins 1 and 2, APLP1 and APLP2 (human), Appl (fly), and apl–1 (worm). They each contain
a large extracellular ... Show more content on Helpwriting.net ...
Additionally, studies have also demonstrated a role for APPs in regulating stem cells. APP
encourages the differentiation of neural stem cells into astrocytic lineage (2). In human embryonic
stem cells, the over expression of APP or its soluble forms causes fast and strong differentiation
towards a neural fate (1). Another function of this protein that have been found in some studies was
that APP was shown to undergo rapid axonal transport to synaptic sites. Moreover, APP was found
in vesicular sections of dendrites and axons. This suggests a possible role for APP in synaptic
function (1). These functions of APP are shown to be involved in neural development. Therefore,
APP is a complex protein that posses many functions, many of which are still not very well
understood.
Fig 1: Summary of the roles of APP and its metabolites during neural development
As mentioned earlier APP is found to be involved in neural development. The functions discussed
above have shown how. During early development, the expression pattern of APP in neuroblasts and
neurons in the neural tube suggests a role in neurogenesis, including neural proliferation,
differentiation and axonal outgrowth (7). Figure 1 shows neural development from early stages. It
shows how APP and APP metabolites play important roles during the different stages of neural
development. The stages range from neural proliferation to the formation of a functional synapse.
The metabolites that posses

What Is The Cause Of Alzheimer's Disease?
Alzheimer's is described as a type of disease that causes mental illness, which causes problems with
memory, thinking, and behavior of an individual. It is a deterioration of the nervous system
especially the neurons in the brain. Alzheimers' is the result of mutations on genes. Specifically,
familial alzheimer's is caused by a mutation in the gene coding for the amyloid precursor protein
(APP) on chromosome 21q.When this gene is modified, a toxic protein fragment called amyloid
beta peptide are produced in the brain. This peptide builds up in the brain and form amyloid plaques.
The accumulation of this "amyloid beta peptide and amyloid plaque," can lead to a great deal of
death of nerve cells and progression of symptoms of Alzheimer's disease (Genetics Home
Reference, paragraph 6). ... Show more content on Helpwriting.net ...
The cases seem to be rising because Alzheimer's progress with increasing age, and with the
advancement of the medical field people are able to live longer, therefore it is expected that
Alzheimer's cases will increase in the time to come. With that being said, Alzheimers is usually
diagnosed by a physician. The physician must take record of family medical history, especially in
changes of cognitive and behavior changes. If suspected of having Alzheimer's doctors usually run
tests such as cognitive tests and physical and neurologic examinations. Contrary, MRI's are done to
analyze the brain, to see if there are other reasons for the symptoms, such as stroke or a brain

Amyloid Synthesis
Amyloid beta (Aβ) is a short peptide contains 37 to 43 amino acids and is well known for its
hypothesized role in causing pathogenesis of AD, since one of the main hallmarks of AD is the
accumulation of fibrillogenic Aβ in the grey matter of the brain (14–15). Meanwhile, over 90% of
AD patients have cerebral amyloid angiopathy (CAA) which is characterized by the deposition of
Aβ in capillaries, arteries, and arterioles (16–17). CAA causes the degeneration of smooth muscle
cells and leads haemorrhages (17).
Aβ is generated by proteolytic processing from its precursor, the amyloid precursor protein (APP),
which is a type–I oriented membrane protein and its splicing variants include APP695, APP714,
APP751, APP770 (18–21). The isoforms APP751 ... Show more content on Helpwriting.net ...
The processing of APP involves three proteases, α–, β–, and γ–secretases and two processing
pathways, the amyloidogenic pathway and the anti–amyloidogenic pathway as shown in Figure 2
(14, 23). The Aβ is generated in amyloidogenic pathway which is mediated by β–, and γ–secretases
(14). The β– secretase first sheds the ectodomain of APP and generates the APP carboxy–terminal
fragment (βCTF) (14). Then the γ–secretase cuts at the transmembrane region of βCTF and releases
the Aβ into the extracellular fluids like cerebrospinal fluid or plasma (14, 24). In the anti–
amyloidogenic pathway α–secretase first cuts at the middle region of Aβ so a trauncated APP CTF
(αCTF) is generated and after the transmembrane cut of γ–secretase, a truncated Aβ peptide is
released (p3) (Figure 2; 25). The amyloidogenic and anti–amyloidogenic competes with each other
(26–27). In addition, when the γ–secretase cuts at the transmembrane region of APP, the cut site is
not restricted to a single position. The γ–secretase first cuts at

Alzheimer's Disease Research Paper
Alzheimer's disease is a degenerative brain disease. It is a form of dementia most common in older
individuals, identifiable to scientists by the presence of amyloid plaques and tau tangles. Most
individuals associate the disease with memory loss, unusual behavior and moods, and watching their
loved ones fade away. While there are recognized genetic risk factors that may contribute to
disease–onset, environmental and lifestyle factors also play a role in disease development. Five FDA
approved medications are currently on the market to treat symptoms, but none are capable of halting
or slowing progression of the disease, nor are they capable of treating underlying causes. Though
there is currently no known cure, scientists are working to ... Show more content on Helpwriting.net
...
There are two important physiological abnormalities that define the disease: amyloid plaques and
tau tangles. Abnormal protein deposits throughout the brain form amyloid plaques and tau tangles.
Amyloid is a normally harmless protein that appears throughout the body. Cleavage of the amyloid
precursor protein by β–secretase and γ–secretase leads to the formation of beta–amyloid, a toxic
version of the protein, which leads to the death of neurons. While the mode of action of beta
amyloid is still not definitively known, a 2012 study by the University of Michigan supports the idea
that it damages neuronal membranes (Moore). According to this theory, the plaques poke tiny holes
in the membrane, allowing calcium to flow into the neuron uncontrollably, leading to the eventual
death of the neuron. Another theory is that the beta amyloid breaks down to form free radicals that
attack the neurons. The degenerated neurons and the amyloid protein combine to form sticky
clumps, known as amyloid plaques, that the body is incapable of breaking down naturally. As a
result, these plaques build up throughout the brain, leading to the loss of connections between
neurons. According to research, plaque formation first occurs in the hippocampus, which plays a
vital role in memory formation. Overtime, additional brain structures are affected, and significant
brain tissue shrinkage

Alzheimer's (ADEOA) Disease Analysis
The autosomal dominant early onset alzheimer's (ADEOA) disease is a mendelian genetic disease.
ADEOA is a form of alzheimer's that affects patients earlier in life, specifically before the age of 65.
Alzheimer's is a form of dementia that causes severe memory, cognitive, and behavior problems,
and results in death normally 10 years after symptoms begin to affect the patient. It is caused by a
mutation in one of the the amyloid precursor protein (APP), presenilin 1 (PSEN1), and or 2
(PSEN2) genes. One mutation is the amyloid precursor protein, located in 21q21.3, found in the
lipocytes in the cerebrum which in diseased patients, produces beta amyloid by improperly dividing.
The beta amyloid is found in the amyloid plaques which are present ... Show more content on
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Some major changes include the shriveling of the cortex, and shrinkage primarily in the
hippocampus. The cortex damage results in limited cognitive and memory abilities, and the
hippocampus shrinkage further destroys the patient's ability to create new

6.3 Amyloid Theory
6.3 Amyloid theory The most commonly supported hypothesis for the cause of AD relates to a
protein expressed in many cells, of unknown function and implicated in familial AD due to
mutations in the gene that code for it(Wisniewski, Wisniewski & Wen 1985). Although its function
is not completely understood, –amyloid precursor protein (APP) is suggested to be critical for
neuron growth(Turner et al. 2003, Vasto et al. 2008, Priller et al. 2006), signalling, and may also
function as an antioxidant(Crouch 2007) and a metalloprotein, modulating copper transport and
metabolism(Turner et al. 2003, Priller et al. 2006, Kong et al. 2007). The parent protein, the 695–
770 amino acid APP, in most cell types undergoes the non–amyloidogenic pathway. Cleavage of the
APP protein can occur at many sites within the cell, including the trans–Golgi network, ... Show
more content on Helpwriting.net ...
The amyloidogenic version of the pathway involves cleavage by –secretase followed by the –
secretase (see figure 6), releasing the 40–43 amino acid amyloid beta (A) peptide, thought to cause
the neurodegenerative disease(Selkoe 2001, Findeis 2007). The enzymatic action of –secretase
leaves a C–terminal fragment known as APP–CTF or
C99, within the membrane and releases APPs into the extracellular space. After A peptide generation
by –secretase from the C99 fragment, the A peptide is extracellularly secreted(Rogaeva et al. 2007).
Most of the A peptides produced are 40 amino acids long, however it is thought in the diseased state
the usual 10% of A peptide production increases, causing havoc within the cell and the surrounding
environment(Vasto et al. 2008). This longer form
(A
42
42
) is more hydrophobic and fibrillates more easily, and is also controversially thought to be more
neurotoxic than the A peptide(Selkoe 2001, Findeis

Alzheimer's Disease Essay
Alzheimer's Disease, progressive brain disorder that causes a gradual and irreversible decline in
memory, language skills, perception of time and space, and, eventually, the ability to care for
oneself. First described by German psychiatrist Alois Alzheimer in 1906, Alzheimer's disease was
initially thought to be a rare condition affecting only young people, and was referred to as presenile
dementia. Today late–onset Alzheimer's disease is recognised as the most common cause of the loss
of mental function in those aged 65 and over. Alzheimer's in people in their 30s, 40s, and 50s, called
early–onset Alzheimer's disease, occurs much less frequently, accounting for less than 10 percent of
the estimated 4 million Alzheimer's cases in the ... Show more content on Helpwriting.net ...
Alzheimer's patients may live many years with the disease, usually dying from other disorders that
may develop, such as pneumonia. Typically the time from initial diagnosis until death is seven to ten
years, but this is quite variable and can range from three to twenty years, depending on the age of
onset, other medical conditions present, and the care patients receive.
The brains of patients with Alzheimer's have distinctive formations–abnormally shaped proteins
called tangles and plaques–that are recognised as the hallmark of the disease. Not all brain regions
show these characteristic formations. The areas most prominently affected are those related to
memory.
Tangles are long, slender tendrils found inside nerve cells, or neurons. Scientists have learned that
when a protein called tau becomes altered, it may cause the characteristic tangles in the brain of an
Alzheimer's patient. In healthy brains, tau provides structural support for neurons, but in Alzheimer's
patients this structural support collapses.
Plaques, or clumps of fibres, form outside the neurons in the adjacent brain tissue. Scientists found
that a type of protein, called amyloid precursor protein, forms toxic plaques when it is cut in two
places. Researchers have isolated the enzyme beta–secretase, which is believed to make one of the
cuts in the amyloid precursor protein. Researchers also identified another enzyme, called gamma
secretase that makes the second cut

Alzheimer 's Disease : Genetic Analysis
Alzheimer's Disease: Genetic Analysis
Introduction
Alzheimer's disease (AD) is a profoundly common form of degenerative dementia that is caused by
neurofibrillary tangles and amyloid plaques accumulating in the brain (Sennvik et.al., 2000). The
study of the human genome has elucidated gene variants; single nucleotide polymorphisms (SNPs)
and mutations which affect the age of onset and the likelihood of developing AD. Understanding the
causes of familial AD, the genetic risk factors for AD and the links between AD and other disorders;
such as Down's syndrome, will aid researchers in the diagnosis and treatment of AD.
Familial Alzheimer 's disease
Familial Alzheimer's disease (FAD) is the inheritable genetic predisposition to early–onset AD. ...
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This promotes the aggregation of amyloid plaques and causes early–onset of FAD.
Presenilin 1 & Presenilin 2
PSEN1 and PSEN2 are polytopic membrane proteins (Davis et.al., 1998) that form the catalytic core
in the protease γ–secretase (Francis et.al., 2002), which is responsible for the proteolysis of APP
(Navivaeva & Turner, 2013). When there is a mutation at the loci for PSEN1 and PSEN2, located on
chromosome 14 and 1 respectively, the activity of γ–secretase is altered resulting in changes in the
proteolysis of APP and increased formation of Aβ (Qain et.al., 1998). Due to the increase of Aβ,
amyloid plaques aggregate quickly causing early–onset of AD.
Amyloid Plaques and Down's Syndrome
Down's syndrome has distinct phenotypic features which include the aggressive early–onset of AD.
This is due to the location of the APP gene; on chromosome 21. The protein APP is triplicated due to
the trisomy of chromosome 21 (Wisniewski et.al., 1985). The triplication of the APP gene causes an
overexpression of APP; 1.5 times more protein is produced compared to persons with two copies of
the APP gene. This ultimately results in high quantities of amyloid plaques due to the larger quantity
of Aβ produced.
Risk Factors for Alzheimer's Disease
While genetic mutations in proteins such as APP and presenilins have been revealed to cause
deterministic

Alzheimer's Disease: How Cognition Decline?
How Cognition Decline?
Main reason for cognition decline could be buildup of plaque and dysfunctional proteins in the brain
interfering with neuronal function. Alzheimer's disease (AD) is an age–related neurodegenerative
disease that accounts for more than 60 % of all dementia cases. The disease is characterized by
cognitive deficits and memory loss through a process that lead to the presence of amyloid–β (Aβ)
plaques and neurofibrillary tangles (NFTs). This plaque is composed of abnormally
hyperphosphorylated tau protein in the brain. Amyloid beta (Aβ or Abeta) is a peptide of 36–43
amino acids, forms amyloid plaques in the brain and are toxic to nerve cells. These peptides result
from the amyloid precursor protein (APP), which is cleaved

A Summary Of Alzheimer Disease
Symptoms of Alzheimer disease are hard to detect due to its similarity to other diseases. One of the
most prominent of Alzheimer disease is memory loss, yet such symptom could be mistaken for old
age or dementia. Due to this unfortunate circumstance, doctors cannot detect Alzheimer disease and
the patients are the one who suffer the most. But now, scientists in Japan had discovered how to
detect Alzheimer disease much sooner than before through blood test. Through the measurement of
amyloid–β proteins and its precursors in the blood, doctors can detect Alzheimer disease sooner.
One of the earliest hallmark of Alzheimer disease is the accumulation of amyloid–β proteins. Prior
to this discovery, in order to measure the proteins, the procedure

Alzheimer's Hypothesis
Did you know that Alzheimer's disease kills more people than both prostate and breast cancer put
together? This neurodegenerative illness is the sixth leading cause of death in the United States, but
not only does Alzheimer's affect the five million Americans living with it. People caring for those
with the disease gave up around eighteen billion of their own hours this past year to provide the
needed service. What's even more staggering is that these caregivers put in these hours without pay.
Alzheimer's is a serious concern to scientists, but the disease is rooted in the most complex,
confusing part of the human body, the brain. This is a reason why an effective cure for the disease
has been unavailable in the past, but new developments ... Show more content on Helpwriting.net ...
It is a degenerative disease, which means it gets worse over time and as of right now, there is no way
to reverse its negative effects. Scientists are not entirely sure what causes Alzheimer's, but the
widely accepted theory is known as the amyloid hypothesis of Alzheimer's. This hypothesis states
that Alzheimer's is caused by a buildup of plaques in the brain that damage or kill neurons. These
plaques form when sticky proteins called amyloid beta clump together. Amyloid beta proteins are
produced when amyloid precursor protein (APP) is chopped into multiple pieces by Beta–site
Amyloid precursor protein Cleaving Enzyme 1 (BACE1) and an enzyme referred to as gamma–
secretase. The process begins with APP, which sticks out from the membranes of cells, is cut by
BACE1, which makes small pieces called sAPP beta, which are unrelated to the development of
Alzheimer's. The small fragment that still remains in the cell membrane is then chopped by gamma–
secretase, giving off amyloid beta. There are two main types of treatments that are being researched
that scientists believe could slow or even completely eliminate Alzheimer's, antibody therapies and
BACE1

Preventative Methods Of Alzheimer's Disease
Preventative Methods of Alzheimer's disease
Now that the disparity between Alzheimer's disease prevalence in men and women, as well as the
different rates of incidence in different countries has been established, it is now applicable to discuss
what can be done to prevent this disease. There are many ways that researchers believe people can
use to prevent Alzheimer's disease. Studies by researchers have found that cannabinoids could
stimulate the brain cells and slow the progression of the disease. Conversely, some believe that
Alzheimer's is impossible to fight, regardless of the precautions taken. This paper will examine
Alzheimer's disease and also explore in depth on the following topics: the prevalence of Alzheimer's
in males vs. ... Show more content on Helpwriting.net ...
Frank Longo said it best when he stated," We have cured Alzheimer's in mice. Why can't we move
that success to people?" (Time Magazine)
There is research that suggests altering the lifestyle can lower the risk of developing Alzheimer's
disease. There are also two more ways that people can stay healthy and they are: using cannabinoids
and avoiding benzodiazepines. The former is found in marijuana and the latter in anxiety, epilepsy,
and sleep medications. In the benzodiazepine study, the researchers took hundreds of Canadian
participants that were over the age of 66 and grouped them based on whether they had ever used
benzodiazepines. This research was conducted by de Gage, Moride, Ducruet, Kurth, Verdoux,
Tournier, Pariente, and Begaud in 2014. The study on cannabinoids, a significant component found
in marijuana, was done by Bachmeier, Beaulieu–Abdelahad, Mullan, and Paris in 2013. These
studies play an essential role in illustrating how this disease can be prevented. There may not be a
definitive cure for those who are already deeply afflicted with this disease, even in the future.
However, examining studies on cannabinoids and benzodiazepines may help those who are in the
early stages or have no clinical signs of Alzheimer's. In regards to the benzodiazepine study, the
participants who did not ever use benzodiazepines were placed in the control group (de Gage 2014).
The main finding of this study was the fact that benzodiazepine use is correlated to

Alzheimer's Disease Abstract
Alzheimer's Disease Zaven A. Ohanian San Joaquin Valley College Abstract This research report
will provide a general overview of Alzheimer's disease. This overview will include background and
history of the disease dating back to its discovery by Alois Alzheimer in Germany. It will provide
in–depth information on the anatomy and pathophysiology of the disease, specifically on the roles of
beta–amyloid plaques and neurofibrillary tangles and on how they progress; what happens as they
progress through the brain. Other topics that will be briefly covered include etiology, epidemiology,
treatment, and prognosis. Alzheimer's Disease Background and History Alzheimer's disease is an
acquired form of dementia that impairs the cognitive and behavioral functions of the patient.
Impairment of these functions severely impacts the individual's capacity to function in social and
occupational settings. There is no cure for Alzheimer's disease and its progression is long and
steady. Alzheimer's disease was first observed by a German psychiatrist named Alois Alzheimer in
1901. Having been intrigued by the behavior of a patient at the Frankfurt Asylum, 51 year old
female Auguste Deter, Alois Alzheimer began monitoring her condition. Dr. Alzheimer observed a
number of symptoms including reduced comprehension and memory, aphasia, disorientation,
unpredictable behavior, paranoia, auditory hallucinations, and pronounced psychosocial impairment
(Maurer, Gerbaldo &Volk, 1997). When

Amyloid Synthesis Essay
Most of the lesions in the brain of an AD patient are from plaques, which consist of beta amyloid
peptides that are derived from APP (amyloid precursor protein) 7. APP (amyloid precursor protein)
is located on the cell membrane and consists of N extracellular terminal, short C intracellular
terminal, a single hydrophobic transmembrane domain and a metal binding site 16, and there are
two ways for APP cleaving (figure 2): The first one is non–amyloidogenic pathway which is done by
α–secretase to form the soluble sAPPα and the membrane bound C83, and then γ–secretase cut the
residue of the membrane part to get p3 and AICD protein 7,17. The second one is amyloidogenic
pathway in which it starts when β–secretase cut the APP to shorter sAPPβ than sAPPα and C99
terminal then γ–secretase cut the c99 to Aβ: Amyloid β (40–42 amino acids), and ACID protein
(plays an important role in gene transcription of the protein that responsible for degradation of the
beta amyloid monomer) then beta amyloid is normally degraded by zinc metalloproteases (NEP,
IDE ) 7,17 (see figure 2) and then LRP1 protein escorts amyloid beta proteins out of the brain
through BBB24. Whereas when the concentration of the mis–regulated metals

A Research Study On Alzheimer 's Disease
Dementia is another term for memory loss and there are a couple types of dementia. This research
paper is about Alzheimer 's Disease (AD) which is a specific type of dementia that is closely related
to aging. AD accounts for 50 to 80 percent of dementia cases. AD usually affects people 65 and
older, but it can start in rare cases around 40 to 50. 5.3 million people in America have been
diagnosed with AD, and almost two thirds of the population that has been diagnosed are women
(Alzheimer 's Association, 2015). Learning about AD can help people understand what really goes
on when someone is suffering from it. It is very important to know the history, deblockedion,
diagnosis, causes, treatment, and the people who are affected by AD. History ... Show more content
on Helpwriting.net ...
Deter had forgotten her own name (Maurer, 1997). In 1910, four years after Dr. Alzheimer's
discovery, a psychiatrist that worked with Dr. Alzheimer published the name of the disease
(Alzheimer's Disease) in the eighth edition of his book Psychiatrie (as cited in Handbook of
Gerontology, 2007). Since then, there have been many more breakthroughs in the research of AD. In
the 1960 's, scientist found a relationship between cognitive decline and the number of plaques in
the brain. In the 1970's AD was documented as the most common type of dementia (Bright Focus
Foundation, 2015). In 1984 another ground breaking discovery was made. In 1984 the Beta–
Amyloid was discovered by George Glenner and Cai 'ne Wong (Alzheimer's Association, 2015). In
the 1990 's a few more discoveries were made, such as complex nerve cells, and genetics coincident,
and AD susceptibility. However, the last decade has been crucial to AD discoveries and experiments.
As technology is always improving, scientists are able to push their limits and experiment more. In
2004, Pittsburgh Compound B (PIB) was created (Alzheimer's Association, 2015). PIB is imaging
software that allows early detection of AD. With all of these discoveries, researchers have learned
how the Central Nervous System (CNS) is affected by AD. AD begins in the Entorhinal Cortex of
the brain (Nia.nih.gov) The Entorhinal

Amyloid Cascade Hypothesis
The amyloid cascade hypothesis is the most widely accepted of the AD pathogenesis hypotheses. Its
principle is that the accumulation of Aβ plays a major role in AD pathogenesis, and the disease is
analyzed as a series of abnormalities in the process and secretion of the amyloid precursor protein
(APP), where an inequality between production and clearance of amyloid β is the triggering event
and the most important factor responsible for other abnormalities observed in AD (Hardy et al,
2002; Cummings et al, 2007). Amyloid β is a peptide with high resistance to proteolytic
degradation. It consists of 37–43 amino acids with different isoforms (Deane et al, 2009). Aβ is the
result of sequential cleavage of the amyloid precursor protein (APP), generating ... Show more
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Autosomal dominant mutations in APP, PSEN1, or PSEN2 that alter APP processing and the
production or self aggregation of Aβ, promote aggregation and accumulation of Aβ in brain causing
early–onset AD (Bertram et al., 2010).
It has been found that the oligomeric forms of Aβ were more dangerous than its monomers, acting
intracellularly and extracellularly leading to the disruption of several downstream mechanisms, such
as the disruption of intracellular calcium homeostasis (Camandola and Mattson, 2011), and
impairments of axonal transport and mitochondrial functions (Decker et al., 2010; Querfurth and
LaFerla, 2010; Sheng and Cai, 2012). In addition, several lines of evidence suggest that Aβ regulates
neuronal and synaptic activities and that its accumulation in the brain causes aberrant network
activity and synaptic depression (Palop and Mucke, 2010). Impairments of inhibitory interneurons
and aberrant stimulation of glutamate receptors result in excitotoxicity, and play important upstream
roles in this pathogenic cascade. These impairments also lead to a positive feedback loop, where
aberrant neuronal activity augments Aβ production, which in turn leads to further neuronal damage
(Palop and Mucke, 2010; Bero et al., 2011; Verret et al.,

What Causes Alzheimer's Disease
For years, researchers have been searching for what causes Alzheimer's. Alzheimer's Disease is a
progressive brain disorder that is irreversible and greatly affects one's thinking skills and memory.
Symptoms of the disease usually emerge during a person's mid–sixties, and is the most common
cause of dementia among the elderly (National Institute on Aging). According to recent research, it
is believed that Alzheimer's is caused due to a build up of a protein, called beta–amyloid. This
protein peptide is toxic and insoluble, and forms more predominantly in particular regions of the
brain, compared to the plaque buildup in a healthy aging person's brain. Beta–amyloid proteins form
from a protein known as amyloid precursor protein (APP), which

Causes Of Dementia

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