Alzheimer's disease is an irreversible progressive brain disorder that causes brain cells to degenerate and die. It is the most common cause of dementia, which is a continuous decline in thinking, behavioral, and social skills that disrupts independent functioning. The disease is named after Dr. Alois Alzheimer, who first identified characteristic brain changes of abnormal clumps and tangled bundles of fibers in a woman who had died of an unusual mental illness. Alzheimer's progresses through mild, moderate, and severe stages, and causes memory loss, mood changes, difficulty communicating, and other cognitive declines. While the exact causes are unknown, age and genetics are major risk factors. Current treatments cannot cure the disease but aim to slow symptoms and maintain quality
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, resulting in loss of memory, imagination and speaking skills, and behavioural changes. Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older.
Alzheimer's is a progressive disease, where dementia symptoms gradually worsen over a number of years. In its early stages, memory loss is mild, but with late-stage Alzheimer's, individuals lose the ability to carry on a conversation and respond to their environment.
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, resulting in loss of memory, imagination and speaking skills, and behavioural changes. Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older.
Alzheimer's is a progressive disease, where dementia symptoms gradually worsen over a number of years. In its early stages, memory loss is mild, but with late-stage Alzheimer's, individuals lose the ability to carry on a conversation and respond to their environment.
A presentation about Alzheimer's disease, it's definition, it's etiology, its mechanism of development as well as actual treatment and developing treatments.
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
Describes about the major neurodegenerative disorders such as Dementia,Alzhimers disease,Parkinsons disease,Amyotrophic lateral sclerosis,etc.Their causes,symptoms and preventative measures.
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 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
Alzheimer's Disease is a progressive disease that retards mental function and memory loss. It includes a whole study about AD an overview, causes, symptoms, Drug treatment, and changes in lifestyle for Alzheimer's Disease.
A presentation about Alzheimer's disease, it's definition, it's etiology, its mechanism of development as well as actual treatment and developing treatments.
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
Describes about the major neurodegenerative disorders such as Dementia,Alzhimers disease,Parkinsons disease,Amyotrophic lateral sclerosis,etc.Their causes,symptoms and preventative measures.
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 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
Alzheimer's Disease is a progressive disease that retards mental function and memory loss. It includes a whole study about AD an overview, causes, symptoms, Drug treatment, and changes in lifestyle for Alzheimer's Disease.
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.
Epidemiology of Alzeimers. Consists of information regarding its global and national burden , its agent ,host and environment ,causes, risk factors and preventive measures to control it.
ALZHEIMER’S DISEASE: IS YOUR POOR MEMORY A WARNING BELL?Meds Engage
Alzheimer’s disease—one of the causative agents of Dementia in the elderly folks is currently the sixth most prominent cause of deaths in America. Dementia results in memory loss, and also affects remembrance, thinking, behavior and cognitive functioning—ultimately hampering the daily routine of the affected person and endangering his or her life.
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.
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
- 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.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
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
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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.
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
3. What is Alzheimer’s?
Irreversible progressive
disorder
causes brain cells to
degenerate --- die
common cause of
dementia
• a continuous decline in
• thinking,
• behavioral
• social skills
disrupts a person's ability
to function independently
60 to 80% dementia cases
4. Dementia vs. Alzheimer’s
Dementia & Alzheimer’s used interchangeably
two conditions aren’t same
Alzheimer’s is a type of dementia.
Dementia is a broader term for conditions with symptoms relating to
memory loss such as forgetfulness and confusion e.g.
• Alzheimer’s disease
• Parkinson’s disease
• traumatic brain injury
5. History
Disease named after Dr. Alois Alzheimer
noticed changes in the brain tissue of a woman
who had died of an unusual mental illness
symptoms
memory loss,
language problems
unpredictable behavior
After she died—examined -- brain --found many abnormal clumps & tangled bundles of fibers
plaques & tangles in brain main features of disease
loss of connections between nerve cells in the brain
damage initially appears be in the hippocampus
7. Stages
• Preclinical: before
symptoms appear
• Mild Cognitive
Impairment: when
symptoms are mild
• Dementia
The
progression
of
Alzheimer's
divided
into three
main stages:
8. Early onset Alzheimer’s
typically affect people age 65Y <
• It can occur in people in early 40s or 50s
• called early onset, or younger onset,
Alzheimer’s
• affects about 5% of all people with the
condition
Symptoms include
• mild memory loss
• trouble concentrating or finishing
everyday tasks
• hard to find the right words
• Mild vision problems
9. Late onset Alzheimer’s
most
common
type
typically
affecting
people age
65 and older
Symptoms
usually worsen
more slowly
than in early-
onset
It may run in
families
but scientists
have not
found
specific
genes
Familial
Alzheimer’s
disease:
This rare type
results from
genetic changes
passed down
from parent to
child.
Familial
Alzheimer’s
makes up less
than 1% of cases
overall but about
60% of early-
onset cases.
10. Causes
exact causes aren't fully
understood
>1% caused by specific
genetic changes
• that fail to function normally
• disrupt the work of neurons
• unleash a series of toxic events.
problems with brain
proteins
Neurons are damaged
lose connections to each
other
eventually die
11. Continue…
The damage most often starts in the region of the brain that controls memory
but the process begins years before the first symptoms
The loss of neurons spreads in a predictable pattern to other regions of the brains
By the late stage of the disease, the brain has shrunk significantly
Researchers are focused on the role of two proteins
• Plaques are deposits of a protein fragment called beta-amyloid that build up in the spaces between
nerve cells
• Tangles are twisted fibers of another protein called tau that build up inside cells
12. Risk Factors
Age
Family History & Genetics
• apolipoprotein E gene (APOE)
• variation of the gene, APOE e4– increase the risk of disease
Down syndrome
Sex
Mild cognitive impairment
Past head trauma
Poor sleep patterns
Lifelong learning and social engagement
Lifestyle and heart health
13. Diagnosis
taking a medical history
They may ask about
your:
• symptoms
• family medical history
• other current or past health
conditions
• current or past medications
• Diet
• alcohol intake
• other lifestyle habits
From there, your doctor
will likely do several tests
to help determine if you
have Alzheimer’s disease
14. Doctors may:-
Ask the person & close relatives Qs about overall health
• use of prescription , medicines, Diet, past medical problems, ability to carry out daily activities, changes in behavior and
personality
Conduct tests of
• memory, problem solving, attention, counting, and language
Carry out standard medical tests
• such as blood and urine tests
• to identify other possible causes of the problem
Perform brain scans, such as CT, MRI, PET
• to rule out other possible causes for symptoms
These tests may be repeated to give doctors information about how the person’s memory and
other cognitive functions are changing over time
15. Preventing Alzheimer’s
Just as there’s no
known cure for
Alzheimer’s, there
are no foolproof
preventive
measures. However,
researchers are
focusing on overall
healthy lifestyle
habits as ways of
preventing cognitive
decline.
The following measures
may help:
• Quit smoking.
• Exercise regularly.
• Try cognitive training exercises.
• Eat a plant-based diet.
• Consume more antioxidants.
• Maintain an active social life.
16. Treatment
no treatment that cures
Alzheimer’s disease is complex, and it is unlikely that any one drug or other intervention
can successfully treat it.
Current approaches focus on helping people
• maintain mental function
• manage behavioral symptoms
• slow down certain problems e.g. memory loss
Researchers hope to develop therapies targeting specific genetic, molecular, and cellular
mechanisms so that the actual underlying cause of the disease can be prevented
17. Statistics
The statistics
surrounding
Alzheimer’s
disease are
daunting. 1 M in cases of
dementia in
Pakistan
10 M people get
dementia every
year globally
Someone is
diagnosed with it
after every 3s.
6th most common cause
of death among U.S.
adults.
It ranks 5th among
causes of death for
people 65 years
and older.
A study found that 4.7 million
Americans <65 years had
Alzheimer’s disease in 2010. Those
researchers projected that by
2050, there will be 13.8 million
Americans with Alzheimer’s.
18. Counseling
Providing information
Helping the individual
cope with decreased
cognitive abilities
addressing the emotional
feelings that are
with having a serious
illness
Improve cognitive function
and performance
This damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As neurons die, additional parts of the brain are affected. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.
In addition, the Alzheimer's Association describes seven stages along a continuum of cognitive decline, based on symptom severity.
The scale ranges from a state of no impairment, through mild and moderate decline, eventually reaching "very severe decline."
A diagnosis does not usually become clear until stage four, described as "mild or early-stage Alzheimer's."
Alzheimer’s typically affects people ages 65 years and older. However, it can occur in people as early as their 40s or 50s. This is called early onset, or younger onset, Alzheimer’s. This type of Alzheimer’s affects about 5 percent of all people with the condition.
Symptoms of early onset Alzheimer’s can include mild memory loss and trouble concentrating or finishing everyday tasks. It can be hard to find the right words, and you may lose track of time. Mild vision problems, such as trouble telling distances, can also occur.
Scientists believe that for most people, Alzheimer's disease is caused by a combination of genetic, lifestyle and environmental factors that affect the brain over time.
Plaques. Beta-amyloid is a leftover fragment of a larger protein. When these fragments cluster together, they appear to have a toxic effect on neurons and to disrupt cell-to-cell communication. These clusters form larger deposits called amyloid plaques, which also include other cellular debris.
Tangles. Tau proteins play a part in a neuron's internal support and transport system to carry nutrients and other essential materials. In Alzheimer's disease, tau proteins change shape and organize themselves into structures called neurofibrillary tangles. The tangles disrupt the transport system and are toxic to cells.
One better understood genetic factor is a form of the apolipoprotein E gene (APOE). A variation of the gene, APOE e4, increases the risk of Alzheimer's disease, but not everyone with this variation of the gene develops the disease.
Many people with Down syndrome develop Alzheimer's disease. This is likely related to having three copies of chromosome 21 — and subsequently three copies of the gene for the protein that leads to the creation of beta-amyloid. Signs and symptoms of Alzheimer's tend to appear 10 to 20 years earlier in people with Down syndrome than they do for the general population.
Mild cognitive impairment (MCI) is a decline in memory or other thinking skills that is greater than what would be expected for a person's age, but the decline doesn't prevent a person from functioning in social or work environments.
People who have MCI have a significant risk of developing dementia. When the primary MCI deficit is memory, the condition is more likely to progress to dementia due to Alzheimer's disease. A diagnosis of MCI enables the person to focus on healthy lifestyle changes, develop strategies to compensate for memory loss and schedule regular doctor appointments to monitor symptoms.
Studies have found an association between lifelong involvement in mentally and socially stimulating activities and a reduced risk of Alzheimer's disease. Low education levels — less than a high school education — appear to be a risk factor for Alzheimer's disease.
The only definitive way to diagnose someone with Alzheimer’s disease is to examine their brain tissue after death. But your doctor can use other examinations and tests to assess your mental abilities, diagnose dementia, and rule out other conditions.
positron emission tomography (PET)
There is no treatment that cures Alzheimer's disease or alters the disease process in the brain. In advanced stages of the disease, complications from severe loss of brain function — such as dehydration, malnutrition or infection — result in death.
Alzheimer’s disease is complex, and it is unlikely that any one drug or other intervention can successfully treat it. Current approaches focus on helping people maintain mental function, manage behavioral symptoms, and slow down certain problems, such as memory loss. Researchers hope to develop therapies targeting specific genetic, molecular, and cellular mechanisms so that the actual underlying cause of the disease can be stopped or prevented.