Alzheimer's disease is a progressive brain disorder that causes memory loss and cognitive decline. The main pathological features are amyloid plaques and neurofibrillary tangles in the brain. Risk factors include age and family history. Symptoms include memory loss, problems with thinking and language, and behavioral changes. A diagnosis is made based on medical history, cognitive tests, and brain imaging. Currently, treatment focuses on managing symptoms with medications and lifestyle changes. Research continues on developing disease-modifying therapies to slow or stop progression.
Molecular Mechanisms of Neurodegeneration: Neurodegenerative Disorders Webin...QIAGEN
Common molecular mechanisms and pathways leading to neurodegeneration, such as Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease or Multiple Sclerosis, are presented in this slideshow. Learn more about research and therapeutic strategies as well as how these discoveries and tools can be used to facilitate your neurodegeneration research.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
1. WHAT IS GENE THERAPY
2. PRINCIPLE OF GENE THERAPY
3. TYPES OF GENE THERAPY
4. VECTORS IN GENE DELIVERY SYSTEM
5. ROLE OF GENE THERAPY IN CNS DISORDERS
6. GENE THERAPY FOR ALZHEIMERS DISEASE
7. GENE THERAPY FOR AMYOTROPIC LATERAL SCLEROSIS
8. GENE THERAPY FOR STROKE
9. CELL THERAPY FOR CNS DISORDERS
10. CELL THERAPY STRATEGIES
11. CELL THERAPY FOR PARKINSON
12. CELL THERAPY FOR HUNTINGTONS DISEASE
13. CRISPR/CAS9
Molecular Mechanisms of Neurodegeneration: Neurodegenerative Disorders Webin...QIAGEN
Common molecular mechanisms and pathways leading to neurodegeneration, such as Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease or Multiple Sclerosis, are presented in this slideshow. Learn more about research and therapeutic strategies as well as how these discoveries and tools can be used to facilitate your neurodegeneration research.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
1. WHAT IS GENE THERAPY
2. PRINCIPLE OF GENE THERAPY
3. TYPES OF GENE THERAPY
4. VECTORS IN GENE DELIVERY SYSTEM
5. ROLE OF GENE THERAPY IN CNS DISORDERS
6. GENE THERAPY FOR ALZHEIMERS DISEASE
7. GENE THERAPY FOR AMYOTROPIC LATERAL SCLEROSIS
8. GENE THERAPY FOR STROKE
9. CELL THERAPY FOR CNS DISORDERS
10. CELL THERAPY STRATEGIES
11. CELL THERAPY FOR PARKINSON
12. CELL THERAPY FOR HUNTINGTONS DISEASE
13. CRISPR/CAS9
A detailed description of programmed cell death mechanism also called Apoptosis.
It explains about the factors, mechanism and pathways involved in the apoptosis.
Pharmacotherapy of Alzheimer's disease
Introduction
History
Risk factors
Pathophysiology
Symptoms
Diagnosis
Non pharmacological treatment
Drugs used in treatment of Alzheimer`s
Recent advances
Screening methods
Summary
References
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
A detailed description of programmed cell death mechanism also called Apoptosis.
It explains about the factors, mechanism and pathways involved in the apoptosis.
Pharmacotherapy of Alzheimer's disease
Introduction
History
Risk factors
Pathophysiology
Symptoms
Diagnosis
Non pharmacological treatment
Drugs used in treatment of Alzheimer`s
Recent advances
Screening methods
Summary
References
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
Alzheimer's disease is a degenerative
brain disorder of unknown etiology which
is the most common form of dementia, that
usually starts in late middle age or in old
age, results in progressive memory loss,
impaired thinking, disorientation, and
changes in personality and mood. There is
degeneration of brain neurons especially in
the cerebral cortex and presence of
neurofibrillary tangles and plaques
containing beta-amyloid cells
The disease was first described
by Dr. Alois Alzheimer, a German
physician, in 1906. Alzheimer had a
patient named Auguste D, in her
fifties who suffered from what
seemed to be a mental illness. But
when she died in 1906, an autopsy
revealed dense deposits, now called
neuritic plaques, outside and around
the nerve cells in her brain. Inside
the cells were twisted strands of
fiber, or neurofibrillary tangles.
Since Dr. Alois Alzheimer's was the
first person who discovered the
disease, AD was named after him.
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
Dementia is an umbrella term that can affect even young individuals. This presentation investigates causes, assessment, diagnosis, and treatment options.
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.
Pathology antioxidants handwritten notes by urooj umeruroojumer1
antioxidants and its types (enzymatic and non-enzymatic ) are discussed in detail with chemical reactions
ROS generation and removal is discussed in detail.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. CONTENTS
What is Alzheimer’s disease
Alzheimer’s vs dementia
Pathology
Pathophysiology
Causes
Signs and symptoms
Diagnosis
Genetics
Neurochemistry
Therapeutic approaches treatment of behavioral symptoms
treatment of cognitive symptoms
Clinical overview
Clinical summary
Inhibition of neurodegeneration
3. WHAT IS ALZHEIMER’S
DISEASE
“IT IS PROGRESSIVE DISORDER THAT CAUSES THE BRAIN CELLS
TO WASTE (DENERATE) ANYWAY AND DIE”
It is the most common cause of DEMENTIA.
IT is an irreversible, progressive brain disorder that slowly destroys
memory and thinking skills and, eventually, the ability to carry out the
simplest tasks
5. ALZHEIMER’S VS DEMENTIA
• Dementia is an umbrella like term
that Alzheimer’s disease fall under.
• Alzheimer’s is the most
common type of dementia.
DEMMENTIA ALZHEIMER’S
It is a general term for decline in
mental ability. It is potentially
reversible.
It is loss of cognitive function of brain.
It is irreversible.
It is non specific because it is due to
many unknown causes.
It is specific because it is due to
known causes.
6. PATHOLOGY
“PHYSICAL CHANGES IN BRAIN LEAD TO THE PATHOLOGY OF
ALZHEIMER’S DISESE .”
The classic pathological signs of Alzheimer’s disease are:
• Amyloid plaques:
Aggregates of misfold proteins that form in spaces between nerve cells.
Accumulation of ß-amyloid protein
• Neurofibrillary tangles:
Insoluble twisted fibers found inside brain cells
Abnormal changes in tau protein
• Inflammation:
Excessive immune response that ends up killing the neurons instead of protecting
them.
Cytokines are boosted
10. PATHOPHYSIOLOGY
• Alzheimer’s disease is associated with brain shrinkage and localized loss of
neurons, mainly in the hippocampus and basal forebrain. The loss of
cholinergic neurons in the hippocampus and frontal cortex is a feature of the
disease.
Some pathological hypothesis clearly explains the pathophysiology of this disease :
Hyperphosphorylated tau protein and amyloid β
hypothesis:
imbalance between β-amyloid (Aβ) production and clearance leads to various
types of toxic oligomers, namely protofibrils, fibrils and plaques depending upon
the extent of oligomerization.
Oxidative stress hypothesis:
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced in
many normal and abnormal processes in humans.
.
11. CONT…
Neuron can interact with ROS, leading to the lipid peroxidation
reaction and molecular apoptosis, in addition, less glutathione in
neurons is also one of the causes of oxidative stress injury.
Metal ion hypothesis:
Changes in the equilibrium of redox transition metals; mainly
copper (Cu), iron (Fe) and other trace metals. Their levels in the
brain are found to be high in AD.
Cholinergic hypothesis:
Cholinergic receptor binding is reduced in specific brain regions
with mild to moderate AD and is related to neuropsychiatric
symptoms.
13. CAUSES
“Alzheimer's disease is thought to be caused by the abnormal
build-up of proteins in and around brain cells.”
• Amyloid plaques
• Neurofibrillary tangles
• Loss of neurons ( neurons of basal forebrain)
• Loss of cholinergic neurons.
• Alzheimer’s disease is a progressive condition, meaning that the
symptoms get worse over time. Memory loss is a key feature, and
this tends to be one of the first symptoms to develop.
14. SIGNS AND SYMPTOMS
• Memory loss that disrupts daily life
• Challenges in planning or solving problems
• Difficulty completing familiar tasks
• Confusion with time or place
• Trouble understanding visual images and spatial
relationships.
• New problems with words in speaking or writing.
• Misplacing things and losing the ability to retrace steps.
• Decreased or poor judgment.
• Withdrawal from work or social activities
• Changes in mood and personality
15.
16. DIAGNOSIS
• Alzheimer disease is often a terrifying diagnosis for both
patients and their families.
• The only definitive way to diagnose Alzheimer’s disease is to
examine brain tissue under the microscope.
• The early stages of Alzheimer's disease are difficult to
diagnose ,a definitive diagnosis is usually made once
cognitive impairment compromises daily life activities.
• To diagnose Alzheimer's, doctors conduct tests to assess
memory impairment and other thinking skills, judge functional
abilities, and identify behavior changes.
17. DIAGNOSTIC TESTS
To assess for Alzheimer’s, there are quick
tests, such as
• Mini-Mental Status Exam (MMSE)
and mini-cog
• CT scan
• MRI
• PET (positron emission tomography)
• CSF examination
• EEG
• SPECT (Single-Photon Emission
Computed Tomography)
• Biomarkers
Technology involving positron
emission tomography (PET),
This imaging technique can spot
amyloid plaques in the brain.
18. GENETICS
• A family history of Alzheimer's disease increases a persons risk of
developing the disease themselves.
• Although environmental factors play a role but studies indicate
that 60-80% of disease is due to genetics.
• There are two types of Alzheimer’s—
1. early-onset
2. late-onset Both types have a genetic component
• Researchers have not found a specific gene that directly causes
late-onset Alzheimer's disease. However, having a genetic variant
of the Apo lipoprotein E (APOE) gene on chromosome 19 does
increase a person's risk
19. GENE MUTATION
The three single-gene mutations associated with early-onset
Alzheimer’s disease are:
i. Amyloid precursor protein (APP) on chromosome 21
ii. Presenilin 1 (PSEN1) on chromosome 14
iii. Presenilin 2 (PSEN2) on chromosome 1
Identification of these genes has led to a number of animal models
that have been useful to study the pathogenesis underlying AD.
20. GENE PROBABILITY
“Probability is used to measure the chances or
likelihood of an event to occur, a hypothesis
being correct, or a scientific prediction being
true”
A child whose biological mother or father carries a genetic
mutation for one of these three genes has a 50/50 chance
of inheriting that mutation. If the mutation is in fact
inherited, the child has a very strong probability of
developing early-onset Alzheimer’s disease.
21. NEUROCHEMISTRY
• The most striking neurochemical disturbance in AD is a
deficiency of ACh.
• The anatomical basis of the cholinergic deficit is atrophy and
degeneration of subcortical cholinergic neurons. can induce a
confusional state.
• AD, however, is complex and also involves multiple
neurotransmitter systems, including GLUTAMATE, 5HT, and
neuropeptides, and there is destruction of not only cholinergic
neurons but also the cortical and hippocampal targets that
receive cholinergic input.
• NOREPINEPHRINE and SOMATOSTATIN are also involved
22.
23. THERAPEUTIC APPROACHES
• Treatment of AD has two approaches :
Treatment of cognitive symptoms
Treatment of behavioral symptoms.
TREATMENT OF
COGNITIVE SYMPTOMS
• Cognitive impairment is when a person has
trouble remembering, learning new things,
concentrating, or making decisions that affect
their everyday life. Cognitive
impairment ranges from mild to severe
24. DRUGS FOR COGNITIVE
SYMPTOMS
Two types of drugs are currently used to treat cognitive symptoms:
• Cholinesterase inhibitors
• Memantine (Namenda)
CHOLINESTRASE INHIBITORS
• Cholinesterase inhibitors. These drugs work by boosting levels of cell-to-cell
communication by preserving a chemical messenger that is depleted in the brain
by Alzheimer's disease. The improvement is modest.
• Cholinesterase inhibitors may also improve neuropsychiatric symptoms, such as
agitation or depression. Commonly prescribed cholinesterase inhibitors include
donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon).
26. MEMANTINE
• Memantine (Namenda). This drug works in another brain
cell communication network and slows the progression of
symptoms with moderate to severe Alzheimer's disease. It's
sometimes used in combination with a cholinesterase
inhibitor.
29. SIDE EFFECTS
COMMON
• CONFUSION
• DIZZINESS
• DOWSINESS
• HEADACHE
• INSOMNIA
• HALLUCINATION
• AGITATION
LESS COMMON
• VOMITING
• ANXIETY
• HYPERTONIA
• CYSTITIS
• INCREASED LABIDO
30. TREATMENT OF BEHAVIORAL
SYMPTOMS
• In addition to cognitive decline, behavioral and psychiatric symptoms in
dementia (BPSD) are common,
• These symptoms include irritability and agitation, paranoia and delusional
thinking, wandering, anxiety, and depression.
• A variety of pharmacological options are also available. Both cholinesterase
inhibitors and memantine reduce some BPSD.
• However ,they do not treat some of the most troublesome symptoms, such as
agitation.
• Benzodiazepines can be used for occasional control of acute agitation.
• Typical antipsychotic haloperidol may be useful for aggression
32. CLINICAL OVERVIEW
AD has three major stages:
1- A “preclinical”
stage during which accumulation of Aβ and tau begins,
before any symptoms appear.
2- An “MCI stage”
with episodic memory loss ( repeated questions,
misplaced items, etc.) that is not severe enough to impair
daily function.
3- A “dementia stage”
with progressive loss of functional abilities.
Death usually ensues within 6–12 years of onset, most often
from a
complication of immobility such as pneumonia or pulmonary
embolism.
33. CLINICAL SUMMARY
• The typical patient with AD presenting in early stages of disease should probably be
treated with a cholinesterase inhibitor.
• Patients and families should be counseled that a realistic goal of therapy is to
induce a temporary reprieve from progression, or at least a reduction in the rate of
decline, rather than long-term recovery of cognition.
• As the disease progresses, memantine can be added to the regimen.
• Behavioral symptoms are often treated with a serotonergic antidepressant .
• Eliminating drugs likely to aggravate cognitive impairments, particularly
anticholinergics, benzodiazepines, and other sedative/hypnotics
34. INHIBITION OF
NEURODEGENERATION
• Inhibitors of β- and γ-secretase have been identified
and are undergoing clinical trials.
• Though they are effective in reducing Aβ formation,
several have proved toxic to the immune system and
gastrointestinal tract, and development has been
halted.
• A-ß plaques bind copper and zinc and metal ions
that promotes dissolution of plaques.