Loading presentation...

Present Remotely

Send the link below via email or IM

Copy

Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.

DeleteCancel

Alzheimer's Disease

No description
by

amin gilani

on 8 July 2014

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Alzheimer's Disease

62
ECG
bpm
Questions ?
What is Alzheimer’s ?
Alzheimer's disease (AD), also known as Senile Dementia. It 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.
It is the most common cause of dementia in people of 65 years and older.​

It Affects 10% of people over the age of 65 and 50% over the age of 85 years.
Approximately 4 million patients in the United States.​
Approximately Annual treatment costs = $100 billion.​
It is the fourth leading cause of death in the United States.

The overwhelming majority of patients live at home and are cared for by family and friends.​
Stages of Alzheimer’s Disease​
Symptoms of Developing A.D
Statistics of Alzheimer’s disease​

Alzheimer's Disease
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.​
- Repeat questions, some problems with expression 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.
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.
Symptoms of Developing A.D
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
Symptoms of Developing A.D

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
Diagnosis of Alzheimer’s Disease
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.​
PET scan of the brain of a person with AD showing a loss of function in the temporal lobe.

Diagnostic Tools
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.​
Etiology of Alzheimer’s Disease
-
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
Microscopy image of a neurofibrillary tangle, conformed by hyperphosphorylated tau protein.
Neuropathology
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. ​
Amyloid Precursor Protein​
- 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.
Symptoms of Developing A.D
The diagnosis can be confirmed with very high accuracy post-mortem when brain material is available and can be examined histologically.
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. ​
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.
Psychological tests for depression are employed, since depression can either be concurrent with AD, an early sign of cognitive impairment, or even the cause.​
Mechanism
- 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
Symptom Management

•Sundowning​
PHARMACOLOGIC​ MEASURES
Non-Pharmocological Measures
•Cognitive enhancement​
•Individual and group therapy​
•Regular appointments​
•Communication with family, caregivers​
•Environmental modification
Treatment Measures:
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).

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.

New treatments:
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.


Alzheimer's disease is characterized 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.​
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.
Tangles (neurofibrillary tangles) are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves. ​

•Hypersexuality
•Sleep disturbances​
•Aggression, agitation​
•Psychoses (delusions, hallucinations)​
RESOURCES FOR MANAGING DEMENTIA

•Attorney for will, conservatorship, estate planning​
•Community: neighbors & friends, aging & mental health networks, adult day care, respite care, home-health agency​
•Organizations: Alzheimer’s Association, Area Agencies on Aging, Councils on Aging​
•Services: Meals-on-Wheels, senior citizen centers

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​
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​

Pharmacological treatment:

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
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.

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.
Check Point:
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?
Summary
Dementia is common in older adults but is NOT an inherent part of aging​
AD is the most common type of dementia, followed by vascular dementia and dementia with Lewy bodies​

Evaluation includes history with informant, physical & functional assessment, focused labs, & possibly brain imaging.​

Primary treatment goals: enhance quality of life, maximize function by improving cognition, mood, behavior​.

Treatment may use both medications and nonpharmacologic interventions​.

Community resources should be used to support patient, family, caregivers.
In conclusion I want to end with a small message ....
New Treatment
Full transcript