This document discusses Alzheimer's disease, including its causes, symptoms, stages of progression, diagnosis, current treatments, and potential new treatments in development. Specifically, it describes how Alzheimer's is characterized by beta-amyloid plaque and tau protein tangle buildup in the brain, outlines the four stages of the disease and their symptoms, and discusses several FDA-approved medications commonly used to treat symptoms, including Aricept, Exelon, Razadyne, and Namenda. It also mentions two new compounds in clinical trials, a beta-secretase inhibitor and NIC5-15, that may help slow the disease's progression.
the feathers of the disease and It is histology
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the feathers of the disease and It is histology
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Startups and other digital innovators in the fight against Alzheimer's Disease, dementia and related disorders. Including a review of relevant scientific research to disinguish real opportunity from quackery.
Definition
Statistics of AD
A brief introduction
Signs and symptoms of AD
NMDA receptors
Classification
Causes
Risk Factors
Pathophysiology
AD… The great unknown
Treatment Options
Future Trends
This presentation was delivered to students at UC San Diego on May 2, 2012 by Dawn DeStefani, BSW, who is the director of programs and services for The Glenner Memory Care Centers in San Diego. Learn more at www.glenner.org.
Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. Alzheimer's disease is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.
Symptoms: Amnesia; Dementia
Diseases or conditions caused: Dementia
Pathophysiology
Pathology
BPharm 2nd Semester
MPharm
Therapeutics
MBBS
A presentation about Alzheimer's disease, it's definition, it's etiology, its mechanism of development as well as actual treatment and developing treatments.
Alzheimer's disease is a causes a progressive loss of brain cells leading to memory loss. In this slide we will learn about its causes,symptoms, pathophysiology, treatment, medication and risk factors.
Alzheimer's disease is a neurodegenerative disorder with severe dementia. Due to the accumulation of Beta-Amyloid proteins acetyl-choline producing neurons are getting degenerated. Alzheimer's disease is one of the most devastating brain disorders of elderly humans. It is an under-treated and under-recognized disease that is becoming a major public health problem.
Alzheimer's disease is a progressive neurologic disorder that causes atrophy of brain cells, leading it to cell death. it is degenerative and progressive illness. Increase in age with sedentary lifestyle and lack of brain storming activities are indirectly leading to mental disorders with cognitive disruptions like dementia and lading up into Alzheimer's, which makes life miserable of client due to dependency. It is essential to keep the elderly active physiologically as well as psychologically. Statistical data of several studies shows the rise in the cases of Alzheimer's disease, which is the highlighting point of concern. Due to increased digitalization and decreased socialization among the human species throughout globe is leading to increased in risk of getting cognitive deficits.
Alzheimer's disease is a progressive condition, which means the symptoms develop gradually over many years and eventually become more severe. It affects multiple brain functions.
The first sign of Alzheimer's disease is usually minor memory problems.
For example, this could be forgetting about recent conversations or events, and forgetting the names of places and objects.
As the condition develops, memory problems become more severe and further symptoms can develop, such as:
confusion, disorientation and getting lost in familiar places
difficulty planning or making decisions
problems with speech and language
problems moving around without assistance or performing self-care tasks
personality changes, such as becoming aggressive, demanding and suspicious of others
hallucinations (seeing or hearing things that are not there) and delusions (believing things that are untrue)
low mood or anxiety
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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2 Case Reports of Gastric Ultrasound
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Alzheimer's disease (AD), also known as Senile Dementia
of the Alzheimer Type (SDAT) or simply Alzheimer’s is
the most common form of dementia. This incurable,
degenerative, terminal disease was first described by a
German psychiatrist and neuropathologist Alois
Alzheimer in 1906 and was named after him.
Alzheimer's disease (AD) is a slowly progressive disease
of the brain that is characterized by impairment of
memory and eventually by disturbances in reasoning,
planning, language, and perception.
Many scientists believe that Alzheimer's disease results
from an increase in the production or accumulation of a
specific protein (beta-amyloid protein) in the brain that
leads to nerve cell death.
3. Generally, it is diagnosed in people over
65 years of age, although the less-prevalent
early onset of Alzheimer’s can occur much
earlier.
In 2006, there were 26.6 million sufferers
worldwide.
Alzheimer’s is predicted to affect 1 in 85
people globally by 2050.
4.
5. 1) Early Stage
This is considered as a mild/early stage and the
duration period is 2-4 years.
Frequent recent memory loss, particularly of
recent conversations and events.
Repeated questions, some problems expressing
and understanding language.
Writing and using objects become difficult and
depression and apathy can occur.
Drastic personality changes may accompany
functional decline.
Need reminders for daily activities and
difficulties with sequencing impact driving early
in this stage.
6. 2) Second stage
This is considered as a middle/moderate stage and the duration
is 2-10 years.
Can no longer cover up problems.
Pervasive and persistent memory loss impacts life across settings.
Rambling speech, unusual reasoning, confusion about current
events, time, and place.
Potential to become lost in familiar settings, sleep disturbances,
and mood or behavioral symptoms accelerate.
Nearly 80% of patients exhibit emotional and behavioral problems
which are aggravated by stress and change.
Slowness, rigidity, tremors, and gait problems impact mobility
and coordination.
Need structure, reminders, and assistance with activities of daily
living.
7. 3) Moderate stage
Increased memory loss and confusion.
Problems recognizing family and friends.
Inability to learn new things.
Difficulty carrying out tasks that involve multiple
steps (such as getting dressed).
Problems coping with new situations.
Delusions and paranoia.
Impulsive behavior.
In moderate AD, damage occurs in areas of the
brain that control language, reasoning,
sensory processing, and conscious thought
8. 4) Last stage
This is considered as the severe stage and the
duration is 1-3 years.
Confused about past and present. Loss of recognition
of familiar people and places
Generally incapacitated with severe to total loss of
verbal skills.
Unable to care for self. Falls possible and immobility
likely.
Problems with swallowing, incontinence, and illness.
Extreme problems with mood, behavioral problems,
hallucinations, and delirium.
Patients need total support and care, and often die
from infections or pneumonia
9. Alzheimer's disease is usually diagnosed clinically
from the patient history, collateral history from
relatives, and clinical observations, based on the
presence of characteristic neurological and
neuropsychological features and the absence of
alternative conditions.
Advanced medical imaging with computed
tomography (CT) or magnetic resonance imaging
(MRI), and with single photon emission computer
tomography (SPECT) or positron emission tomography
(PET) can be used to help exclude other cerebral
pathology or subtypes of dementia.
The diagnosis can be confirmed with very high
accuracy post-mortem when brain material is
available and can be examined histologically.
10. .
PET scan of the brain of a person with AD showing a loss
of function in the temporal lobe.
11. Neuropsychological tests such as the mini-mental state
examination (MMSE) are widely used to evaluate the
cognitive impairments needed for diagnosis. More
comprehensive test arrays are necessary for high reliability
of results, particularly in the earliest stages of the
disease.
Psychological tests for depression are employed, since
depression can either be concurrent with AD, an early sign
of cognitive impairment, or even the cause.
When available as a diagnostic tool, SPECT and PET
neuroimaging are used to confirm a diagnosis of
Alzheimer's in conjunction with evaluations involving
mental status examination. In a person already having
dementia, SPECT appears to be superior in differentiating
Alzheimer's disease from other possible causes, compared
with the usual attempts employing mental testing and
medical history analysis.
12. Scientists don’t yet fully understand what causes AD, but it
is clear that it develops because of a complex series of
events that take place in the brain over a long period of
time. It is likely that the causes include genetic,
environmental, and lifestyle factors.
Some drug therapies propose that AD is caused by reduced
synthesis of the neurotransmitter acetylcholine.
Other cholinergic effects have also been proposed, for
example, initiation of large-scale aggregation of amyloid
leading to generalized neuroinflammation.
Alzheimer's disease is characterized by a build-up of
proteins in the brain. Though this cannot be measured in a
living person, extensive autopsy studies have revealed this
phenomenon. The build-up manifests in two ways:
Plaques– deposits of the protein beta-amyloid that
accumulate in the spaces between nerve cells
Tangles – deposits of the protein tau that
accumulate inside of nerve cells
13. Microscopy image of a neurofibrillary tangle, conformed by
hyperphosphorylated tau protein.
14. Alzheimer's disease is characterised by loss of neurons and
synapses in the cerebral cortex and certain subcortical regions.
This loss results in gross atrophy of the affected regions,
including degeneration in the temporal lobe and parietal lobe,
and parts of the frontal cortex and cingulate gyrus.
Both amyloid plaques and neurofibrillary tangles are clearly
visible by microscopy in brains of those afflicted by AD.
Plaques are dense, mostly insoluble deposits of amyloid – beta
peptides and cellular material outside and around neurons.
Tangles (neurofibrillary tangles) are aggregates of the
microtubule-associated protein tau which has become
hyperphosphorylated and accumulate inside the cells themselves.
Although many older individuals develop some plaques and
tangles as a consequence of ageing, the brains of AD patients
have a greater number of them in specific brain regions such as
the temporal lobe.
15. Alzheimer's disease has been identified as a protein misfolding disease
(proteopathy), caused by accumulation of abnormally folded A-beta and tau
proteins in the brain. Plaques are made up of small peptides, 39–43 amino acids in
length, called beta-amyloid (also written as A-beta or Aβ).
Beta-amyloid is a fragment from a larger protein called amyloid precursor protein
(APP), a transmembrane protein that penetrates through the neuron's membrane.
APP is critical to neuron growth, survival and post-injury repair. In Alzheimer's
disease, an unknown process causes APP to be divided into smaller fragments by
enzymes through proteolysis.
One of these fragments gives rise to fibrils of beta-amyloid, which form clumps that
deposit outside neurons in dense formations known as senile plaques.
AD is also considered a tauopathy due to abnormal aggregation of the tau protein.
Every neuron has a cytoskeleton, an internal support structure partly made up of
structures called microtubules.
These microtubules act like tracks, guiding nutrients and molecules from the body
of the cell to the ends of the axon and back. A protein called tau stabilizes the
microtubules when phosphorylated, and is therefore called a microtubule-
associated protein.
In AD, tau undergoes chemical changes, becoming hyperphosphorylated; it then
begins to pair with other threads, creating neurofibrillary tangles and disintegrating
the neuron's transport system.
16. Enzymes act on the APP (amyloid precursor protein) and
cut it into fragments. The beta-amyloid fragment is crucial
in the formation of senile plaques in AD.
17. Exactly how disturbances of production and aggregation of the
beta amyloid peptide gives rise to the pathology of AD is not
known. The amyloid hypothesis traditionally points to the
accumulation of beta amyloid peptides as the central event
triggering neuron degeneration. Accumulation of aggregated
amyloid fibrils, which are believed to be the toxic form of the
protein responsible for disrupting the cell's calcium ion
homeostasis, induces programmed cell death (apoptosis).It is
also known that Aβ selectively builds up in the mitochondria in
the cells of Alzheimer's-affected brains, and it also inhibits
certain enzyme functions and the utilization of glucose by
neurons.
Various inflammatory processes and cytokines may also have a
role in the pathology of Alzheimer's disease. Inflammation is a
general marker of tissue damage in any disease, and may be
either secondary to tissue damage in AD or a marker of an
immunological response.
Alterations in the distribution of different neurotrophic factors
and in the expression of their receptors such as the brain derived
neurotrophic factor (BDNF) have been described in AD
18.
19. Apolipoprotein E (APOE) found on
chromosome 19 appears to be a predisposing
genetic risk factor for the late on-set of AD –
the most typical AD.
APOE helps carry cholesterol in the
bloodstream.
APOE comes in several different forms, or
alleles.
Three forms—APOE ε2, APOE ε3, and APOE ε4
—occur most frequently.
20.
21. Aricept Used to delay or slow the symptoms of AD
Donepezil • Loses its effect over time
• Used for mild, moderate and severe AD
• Does not prevent or cure AD
Celexa
Citalopram Used to reduce depression and anxiety
• May take 4 to 6 weeks to work
• Sometimes used to help people get to sleep
Depakote Used to treat severe aggression
Sodium Valproate • Also used to treat depression and anxiety
Exelon Used to delay or slow the symptoms of AD
Rivastigmine • Loses its effect over time
• Used for mild to moderate AD
• Can get in pill form or as a skin patch
• Does not prevent or cure AD
22. Namenda Used to delay or slow the symptoms of AD
Memantine • Loses its effect over time
• Used for moderate to severe AD
• Sometimes given with Aricept®, Exelon®
• Does not prevent or cure AD
Razadyne Used to prevent or slow the symptoms of
AD
Galantamine • Loses its effect over time
• Used for mild to moderate AD
• Can get in pill form or as a skin patch
• Does not prevent or cure AD
Zoloft Used to reduce depression and anxiety
Sertraline • May take 4 to 6 weeks to work
• Sometimes used to help people get to
sleep
Trileptal Used to treat severe aggression
Oxcarbazepine • Also used to treat depression and anxiety
Tegretol Used to treat severe aggression
Carbamazepine • Also used to treat depression and anxiety
Remeron Used to reduce depression and anxiety
Mirtazepine • May take 4 to 6 weeks to work
• Sometimes used to help people get to
sleep
23. Although there is currently no way to cure
Alzheimer's disease or stop its progression,
researchers are making encouraging advances in
Alzheimer's treatment, including medications and
non-drug approaches to improve symptom
management.
Mild/Moderate AD:
Cholinesterase inhibitors increase the levels of
acetylcholine in the brain, which plays a key role in
memory and learning. This kind of drug postpones the
worsening of symptoms for 6 to 12 months in about
half of the people who take it. Cholinesterase
inhibitors most commonly prescribed for mild to
moderate Alzheimer's disease include Aricept
(donezepil HCL), Exelon (rivastigmine), and Razadyne
(galantamine).
24. Moderate/Severe AD:
Namenda (memantine) regulates glutamate
in the brain, which plays a key role in
processing information. This drug is used to
treat moderate to severe Alzheimer's disease
and may delay the worsening of symptoms in
some people. It may allow patients to
maintain certain daily functions a little
longer than they would without the
medication.
25. Razadyne
Razadyne (galantamine HBr) is FDA-approved for mild and
moderate stages of the disease.
Razadyne is a cholinesterase inhibitor that prevents the
breakdown of acetylcholine in the brain. Acetylcholine
plays a key role in memory and learning; higher levels in
the brain help nerve cells communicate more efficiently.
Razadyne also stimulates nicotinic receptors to release
more acetylcholine in the brain.
26. Razadyne delays the worsening of
Alzheimer's symptoms for 6 to 12 months in
about half of the people who take it.
Razadyne is available in tablet and capsule
form, and is commonly started at 4 mg twice
a day. If it's well tolerated after 4 weeks, the
dosage may be increased to 8 mg twice a
day.
Razadyne also comes in an extended release,
once-a-day tablet.
Razadyne is available in generic form
(galantamine HBr).
27. Exelon (Rivastigmine)
Exelon is FDA approved for mild and moderate stages of
the disease; it is also approved for the treatment of
mild to moderate dementia due to Parkinson's disease.
Exelon is available as a capsule, liquid, and patch.
28. Exelon is a cholinesterase inhibitor that
prevents the breakdown of acetylcholine
and butyrylcholine in the brain by
blocking the activity of two different
enzymes. Acetylcholine and
butyrylcholine play a key role in memory
and learning.
When given orally, bioavailability is about
40% in the 3 mg dose. The compound can
cross the blood-brain barrier.
29. Aricept (Donepizel)
One of the most widely used drugs to treat
the symptoms of Alzheimer's disease. Aricept
is FDA-approved for mild, moderate, and
severe stages of the disease.
30. Aricept is available in tablet form or an
orally disintegrating tablet form, and is
commonly started at 5 mg a day.
Can cross the blood-brain barrier.
31. Namenda (Memantine)
Namenda is an N-methyl D-aspartate (NMDA)
antagonist that regulates the activity of
glutamate in the brain. Glutamate plays a
key role in memory and learning, but excess
glutamate can lead to the disruption of nerve
cell communication or nerve cell death.
32. Studies involving Namenda have shown that
the drug can slow the rate of decline in
thinking and the ability to perform daily
activities in individuals who have moderate
to severe Alzheimer's disease
A dysfunction of glutamatergic
neurotransmission is thought to be involved
in the etiology of AD.
Namenda is available in generic form
(memantine HCL).
33. A molecule designed by a Purdue University researcher to
stop the debilitating symptoms of Alzheimer's disease has
been shown in its first phase of clinical trials to be safe
and to reduce biomarkers for the disease.
The molecule, called a beta-secretase inhibitor, prevents
the first step in a chain of events that leads to amyloid
plaque formation in the brain. This plaque formation
creates fibrous clumps of toxic proteins that are believed
to cause the devastating symptoms of Alzheimer's.
Researchers at Mount Sinai School of Medicine have found
that a compound called NIC5-15, might be a safe and
effective treatment to stabilize cognitive performance in
patients with mild to moderate Alzheimer's disease. The
two investigators, Giulio Maria Pasinetti, M.D., Ph.D. , and
Hillel Grossman, M.D., presented Phase IIA preliminary
clinical findings at the Alzheimer's Association 2009
International Conference on Alzheimer's Disease (ICAD) in
Vienna on July 12.
34. NIC5-15's potential to preserve cognitive
performance will be further evaluated in a
Phase IIB clinical trial. Early evidence
suggests that NIC5-15 is a safe and tolerable
natural compound that may reduce the
progression of Alzheimer's disease-related
dementia by preventing the formation of
beta-amyloid plaque, a waxy substance that
accumulates between brain cells and impacts
cognitive function.
37. An Introduction to Medicinal Chemistry by
Graham L. Patrick, pp. 589-590.
Abbott, Alison. Neuroscience: The plaque
plan. Nature (London, United Kingdom)
(2008), 456(7219), 161-164.
Bolognesi, Maria L.; Matera, Riccardo;
Minarini, Anna; Rosini, Michela; Melchiorre,
Carlo. Alzheimer's disease: new approaches
to drug discovery. Current Opinion in
Chemical Biology (2009), 13(3), 303-308.
38. What are the three stages of Alzheimer’s
Disease?
What are some of the diagnostic tools of
diagnosing Alzheimer’s Disease?
What drugs are used to treat mild/moderate
Alzheimer’s Disease?
Which drug is most commonly used to treat
Alzheimer’s Disease?
Have current pharmaceutical agents been
successful in slowing the progress of
Alzheimer’s Disease?
Why is it important to develop ‘biomarkers’
for Alzheimer’s Disease?