- Alzheimer's disease is a progressive brain disease that destroys memory and thinking skills, and is the most common cause of dementia among older adults.
- The disease is caused by beta-amyloid plaques and neurofibrillary tangles that build up in the brain, and it slowly spreads and causes shrinkage of affected brain regions over time.
- Researchers are studying the causes of Alzheimer's including genetics, lifestyle factors, and are searching for improved treatments through clinical trials and drug research to stop the progression and symptoms of the disease.
Early-onset Alzheimer's disease occurs in people age 30 to 60.
Rare, representing less than 5 percent of all people who have Alzheimer's Inherited type known as familial Alzheimer's disease (FAD). It caused by mutations in at least 3 genes ( these Mutations increase the production of a Aβ42) :Most cases of Alzheimer's are the late-onset form, which develops after age 60.
The causes include a combination of genetic, environmental, and lifestyle factors .
the increase risk is related to the apolipoprotein E (APOE) found gene on chromosome 19.
APOE contains the instructions for making a protein that helps carry cholesterol and other types of fat in the bloodstream. APOE comes in different forms, or alleles. Three forms—APOE ε2, APOE ε3, and APOE ε4—occur most frequently.
APOE ε2 is relatively rare and may provide some protection against the disease.
If Alzheimer's disease occurs in a person with this allele, it develops later in life than it would in someone with the APOE ε4 gene.
Early-onset Alzheimer's disease occurs in people age 30 to 60.
Rare, representing less than 5 percent of all people who have Alzheimer's Inherited type known as familial Alzheimer's disease (FAD). It caused by mutations in at least 3 genes ( these Mutations increase the production of a Aβ42) :Most cases of Alzheimer's are the late-onset form, which develops after age 60.
The causes include a combination of genetic, environmental, and lifestyle factors .
the increase risk is related to the apolipoprotein E (APOE) found gene on chromosome 19.
APOE contains the instructions for making a protein that helps carry cholesterol and other types of fat in the bloodstream. APOE comes in different forms, or alleles. Three forms—APOE ε2, APOE ε3, and APOE ε4—occur most frequently.
APOE ε2 is relatively rare and may provide some protection against the disease.
If Alzheimer's disease occurs in a person with this allele, it develops later in life than it would in someone with the APOE ε4 gene.
What's Alzheimer's its a presentation which i did for a English course at KU Leuven, its very short but it touches the main points of this dementia. It contains What's Alzheimer's, it's symptoms, stages, risk factors and more. Hopefully can be helpful to you.
Recent advances of alzheimer's disease boc sciencesBOC-Sciences
Alzheimer's is a type of dementia that causes problems with memory, thinking and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Here, we sort out the recent advences of Alzheimer's Disease.
Alzheimer's is the most common form of dementia, a general term for memory loss and other intellectual abilities serious enough to interfere with daily life. Alzheimer's disease accounts for 60 to 80 percent of dementia cases.
Disorders of amino acid metabolism
Disorders of renal amino acid transport
Disorders of carbohydrate metabolism and transport
Carbohydrate-deficient protein syndromes
carbohydrate metabolism and transport
Disorders of fatty acid oxidation
Disorders of purine and pyrimidine metabolism
Disorders of lipid and lipoprotein metabolism
Ceroid lipofuscinosis and other lipidoses.
Disorders of serum lipoproteins
Lysosomal disorders
Peroxisomal disorders
Disorders of metal metabolism
Porphyrias
What's Alzheimer's its a presentation which i did for a English course at KU Leuven, its very short but it touches the main points of this dementia. It contains What's Alzheimer's, it's symptoms, stages, risk factors and more. Hopefully can be helpful to you.
Recent advances of alzheimer's disease boc sciencesBOC-Sciences
Alzheimer's is a type of dementia that causes problems with memory, thinking and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Here, we sort out the recent advences of Alzheimer's Disease.
Alzheimer's is the most common form of dementia, a general term for memory loss and other intellectual abilities serious enough to interfere with daily life. Alzheimer's disease accounts for 60 to 80 percent of dementia cases.
Disorders of amino acid metabolism
Disorders of renal amino acid transport
Disorders of carbohydrate metabolism and transport
Carbohydrate-deficient protein syndromes
carbohydrate metabolism and transport
Disorders of fatty acid oxidation
Disorders of purine and pyrimidine metabolism
Disorders of lipid and lipoprotein metabolism
Ceroid lipofuscinosis and other lipidoses.
Disorders of serum lipoproteins
Lysosomal disorders
Peroxisomal disorders
Disorders of metal metabolism
Porphyrias
Global Medical Cures™ | Primer on ALZHEIMERS DISEASE
DISCLAIMER-
Global Medical Cures™ does not offer any medical advice, diagnosis, treatment or recommendations. Only your healthcare provider/physician can offer you information and recommendations for you to decide about your healthcare choices.
Hello,
I am delighted to have the chance to introduce myself to you. My name is Najma AbdiKani, and I am currently pursuing my studies as a nurse student at EAU University. Thank you for taking the time to consider this introduction.
Best regards,
Najma AbdiKani
POWERPOINT PRESENTATION ON PATHOPHYSIOLOGY OF ALZHEIM.docxstilliegeorgiana
POWERPOINT PRESENTATION ON:
PATHOPHYSIOLOGY OF ALZHEIMER'S DISEASE
TANIA GONZALEZ DIAZ
WALDEN UNIVERSITY
NURS:6501C
AUGUST 03,2019
*
Alzheimer’s disease
Alzheimer disease (AD) is: Chronic neurodegenerative disorder
The leading cause of dementia
According to Etindele Sosso, Nakamura & Nakamura (2017), as of 2015, 29.8 million people had AD.
Most prevalent among people whose ages are 65 years and above.
Alzheimer disease (AD) is a chronic neurodegenerative disorder that normally starts and gradually progresses with the brain cells dying off. Leading to memory loss. The leading cause of dementia which affects an individual cognitive, social and behavioral skills that destroy the capability of a person to function properly.According to Etindele Sosso, Nakamura & Nakamura (2017), as of 2015, there were 29.8 million people globally who had AD. It mostly starts in people whose ages are over 65 years.
*
Pathophysiology of Alzheimer’s Disease Exact cause is unknown. Early onset of Familial Alzheimer’s Disease is associated with 3 genes found in chromosome 21, namely; Abnormal amyloid precursor protein 14 [APP14] Abnormal presenilin 1 [PSEN1] andAbnormalpresenilin 2 [PSEN2])Late onset of AD is related to changes in apolipoprotein E gene-allele4(APOE4) gene found in chromosome 19. Source: (Huether, McCance, Brashers & Rote, 2016)
The exact cause of AD is still unknown till date. Early onset of Familial Alzheimer’s Disease is associated with 3 genes found in chromosome 21, namely; Abnormal amyloid precursor protein 14 [APP14] Abnormal presenilin 1 [PSEN1] andAbnormalpresenilin 2 [PSEN2])Late onset of AD is related to changes in apolipoprotein E gene-allele 4 (APOE4) gene found in chromosome 19.
*
Pathophysiology of Alzheimer’s Disease …contdDNA methylation is one epigenetic markers for AD.Pathological alterations in the brain causes the loss of memory.These pathological alterations include; Accumulation of extracellular neuritic plaques with core of amyloid Degeneration of basal forebrain ß-protein Intraneuronal neurofibrillary tanglescholinergic neurons with loss of acetylcholineSource: (Huether, McCance, Brashers & Rote, 2016)
DNA methylation is one epigenetic markers for AD.Pathological alterations in the brain causes the loss of memory.These pathological alterations include; Accumulation of extracellular neuritic plaques with core of amyloid ß-protein Intraneuronal neurofibrillary tanglesDegeneration of basal forebrain cholinergic neurons If the brain is unable to get rid of amyloid the precursor protein, toxic fragments of amyloid ß-protein accumulates and which trigger neuritic plaques to diffuse, the transmission of impulses by nerve cells to be disrupted and the nerve cells to die. The tau protein in neiurons detaches forming an insoluble neurofibrillary tangles, which causes the neurons to die. Neurofibrilary tangles and neuritic plaques which are more concentrated in the cerebral cortex are the one that contribute t ...
This is a presentation I did last spring in which I discuss how the OTPF applies to Alzheimer's Dementia. I collected data from scholarly as well as non-scholarly resources. I hope you find this to be helpful.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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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
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
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
1. National Institute on Aging
National Institutes of Health
ALZHEIMER’S DISEASE
UnravelingtheMystery
2. The Impact of AD
Once considered a rare disorder,
Alzheimer’s disease is now seen as a
major public health problem that is
seriously affecting millions of older
Americans and their families.
The Federal government’s lead agency for Alzheimer’s
disease research is the National Institute on Aging, part of
the National Institutes of Health. NIH is part of the U.S.
Department of Health and Human Services.
Slide 2
3. Alzheimer’s disease is an
irreversible, progressive brain
disease that slowly destroys
memory and thinking skills.
What is AD?
Although the risk of developing AD increases with age – in
most people with AD, symptoms first appear after age 60 –
AD is not a part of normal aging. It is caused by a fatal
disease that affects the brain.
Slide 4
4. What is AD?
AD Statistics….
• AD is the most common
cause of dementia among
people age 65 and older.
• Scientists estimate that
around 4.5 million people
now have AD.
• For every 5-year age
group beyond 65, the
percentage of people with
AD doubles.
• By 2050, 13.2 million older
Americans are expected to have
AD if the current numbers hold
and no preventive treatments
become available.
Slide 5
5. What is AD?
Where are people with AD cared for?
• home
• assisted living facilities (those in
the early stages)
• nursing homes (special care units)
• The national cost of caring for
people with AD is about $100
billion every year.
Slide 6
6. AD and the Brain
Plaques and Tangles: The Hallmarks of AD
The brains of people with AD have an abundance of two
abnormal structures:
• beta-amyloid plaques, which are dense deposits of protein and
cellular material that accumulate outside and around nerve
cells
• neurofibrillary tangles, which are twisted fibers that build up
inside the nerve cell
An actual AD plaque An actual AD tangle
Slide 16
7. Beta-amyloid Plaques
Amyloid precursor protein (APP) is the
precursor to amyloid plaque.
1. APP sticks through the neuron
membrane.
2. Enzymes cut the APP into fragments
of protein, including beta-amyloid.
3. Beta-amyloid fragments come together
in clumps to form plaques.
1.
2.
3.
AD and the Brain
In AD, many of these clumps form,
disrupting the work of neurons. This
affects the hippocampus and other areas
of the cerebral cortex.
Slide 17
8. AD and the Brain
Neurofibrillary
Tangles
Neurons have an internal support structure partly made up of
microtubules. A protein called tau helps stabilize microtubules. In AD,
tau changes, causing microtubules to collapse, and tau proteins clump
together to form neurofibrillary tangles.
Slide 18
9. The Changing Brain in
Alzheimer’s Disease
No one knows what causes AD to begin,
but we do know a lot about what happens
in the brain once AD takes hold.
Pet Scan of
Normal Brain
Pet Scan of Alzheimer’s
Disease Brain
AD and the Brain
Slide 19
10. Preclinical AD • Signs of AD are first noticed in
the entorhinal cortex, then
proceed to the hippocampus.
• Affected regions begin to shrink
as nerve cells die.
• Changes can begin 10-20 years
before symptoms appear.
• Memory loss is the first sign of
AD.
AD and the Brain
Slide 20
11. Mild to Moderate AD
• AD spreads through the brain. The
cerebral cortex begins to shrink as
more and more neurons stop
working and die.
• Mild AD signs can include memory
loss, confusion, trouble handling
money, poor judgment, mood
changes, and increased anxiety.
• Moderate AD signs can include
increased memory loss and
confusion, problems recognizing
people, difficulty with language
and thoughts, restlessness,
agitation, wandering, and repetitive
statements.
AD and the Brain
Slide 21
12. Severe AD
• In severe AD, extreme shrinkage
occurs in the brain. Patients are
completely dependent on others for
care.
• Symptoms can include weight loss,
seizures, skin infections, groaning,
moaning, or grunting, increased
sleeping, loss of bladder and bowel
control.
• Death usually occurs from
aspiration pneumonia or other
infections. Caregivers can turn to a
hospice for help and palliative care.
AD and the Brain
Slide 22
13. AD Research: Finding New Answers
and Asking Better Questions
• The Search for Causes (slides 24 – 28 )
• Diagnosing AD (slides 29 – 30)
• Clinical Trials (slide 31)
• The Search for Treatments (slides 32-33)
• New NIA Study (slide 34)
• Managing the Symptoms of AD (slide 35)
Slide 23
14. AD Research: the
Search for Causes
AD develops
• AD develops when genetic, lifestyle, and environmental
factors work together to cause the disease process to start.
• In recent years, scientists have discovered genetic links to
AD. They are also investigating other factors that may
play a role in causing AD. NIA-funded Alzheimer’s
Disease Centers (ADCs) across the country are leading
the research efforts looking into causes, diagnosis, and
treatment of AD.
Slide 24
15. AD Research: the Search for Causes
Genetic Studies
The two main types of AD are
early-onset and late-onset:
• Early-onset AD is rare, usually
affecting people aged 30 to 60
and usually running in families.
Researchers have identified
mutations in three genes that
cause early-onset AD.
• Late-onset AD is more
common. It usually affects
people over age 65.
hRaevsee airdcehnetrifsi ed a gene that produces a protein called apolipoprotein E (ApoE).
Scientists believe this protein is involved in the formation of beta-amyloid
plaques.
Slide 25
16. AD Research: the Search for Causes
Late-onset AD
Genetics Study
• Partnership between the NIA and the
Alzheimer’s Association
• Need to recruit a total of 1,000 families to
find the remaining late-onset risk factor
genes
• 2 or more living siblings with AD
• One other living family member with or
without AD
• Contact: e-mail: alzstudy@iupui.edu or
Website: www.ncrad.org
Slide 26
17. AD Research: the Search for Causes
Studies at the Cellular and
Molecular Level
• Oxidative damage from free
radical molecules can injure
neurons.
• Homocysteine, an amino acid, is a risk factor for heart disease. A study
shows that an elevated level of homocysteine is associated with
increased risk of AD.
• Scientists are also looking at inflammation in certain regions of the
brain and strokes as risk factors for AD.
Slide 27
18. AD Research: the Search for Causes
Epidemiologic Studies
Scientists examine characteristics, lifestyles, and disease
rates of groups of people to gather clues about possible
causes of AD. The NIA is currently funding epidemiologic
studies in a variety of different groups. Two of the studies
focus on religious communities. Researchers conduct
yearly exams of physical and mental status, and studies of
donated brains at autopsy. Some early results indicate:
• Mentally stimulating activity protects the brain in some
ways.
• In early life, higher skills in grammar and density of ideas
are associated with protection against AD in late life.
Slide 28
19. AD Research: Diagnosing AD
Experienced physicians in specialized AD
centers can now diagnose AD with up to 90
percent accuracy. Early diagnosis has
advantages:
• Doctors can rule out other conditions
that may cause dementia.
• If it is AD, families have more time to
plan for the future.
• Treatments can start earlier, when they
may be more effective.
• It helps scientists learn more about the
causes and development of AD.
Slide 29
20. AD Research: Diagnosing AD
Physicians today use a number
of tools to diagnose AD:
• a detailed patient history
• information from family and
friends
• physical and neurological
exams and lab tests
• neuropsychological tests
• imaging tools such as CT scan,
or magnetic resonance imaging
(MRI). PET scans are used
primarily for research purposes
Slide 30
21. AD Research: Clinical Trials
Clinical trials are the primary way
that researchers find out if a
promising treatment is safe and
effective.
• Trials examine approved drugs
to see if they can be used for
other purposes, or look at
experimental drugs.
• Participating in a trial means
regular contact with the study
team, who can provide state-of-the-
art AD care.
Slide 31
22. AD Research: the Search for Treatments
Drugs used to treat mild to moderate AD symptoms include:
• Aricept
• Exelon
• Reminyl
An additional drug, Namenda, has been approved to treat symptoms of
moderate to severe AD. These drugs can help improve some patients’
abilities to carry out activities up to a year or so, but they do not stop or
reverse AD.
Scientists are also studying agents that someday may be
useful in preventing AD. For example, they have
experimented with a vaccine against AD. Although the
first clinical trial was stopped due to side effects in some
participants, valuable information was gathered.
Slide 32
23. AD Research: the Search for New Treatments
Researchers also are looking at other treatments,
including:
• cholesterol-lowering drugs called
statins
• anti-oxidants (vitamins) and folic acid
• anti-inflammatory drugs
• substances that prevent formation of
beta-amyloid plaques
• nerve growth factor to keep neurons
healthy
Slide 33
Editor's Notes
The National Institute on Aging presents: Alzheimer’s Disease, Unraveling the Mystery.
The National Institute on Aging is part of the National Institutes of Health
U.S. Department of Health and Human Services