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About Alzheimer's Disease There is no known cause, but most experts agree that AD develops as a result of multiple factors,

, not a single cause. Alzheimer's disease is the 5th leading cause of death for people ages 65&up in the US 1 in 8 older Americans has AD The healthy adult has 100 billion neurons, and 100 trillion synapses. Beta-amyloid protein causes plaque buildup outside of neurons Tau protein forms tangles inside of the actual neuron, blocking synapses 1st identified over a century ago, but only gained momentum in research about 30 years ago Brain cell disruption usually begins in the hippocampus (in the cortex) where new memory formation occurs, causing short term memory loss. Damage spreads, creating other difficulties Risk Factors Apolipoprotein-E epsilon 4 abnormalities. It's the gene for the protein that carries cholesterol in blood Mild Cognitive Impairment (MCI) Cardiovascular disease (creates a lack of blood to the brain) -Physical inactivity -High cholesterol -diabetes -obesity -smoking Social Engagement and Diet -Social isolation encourages loss -Healthy diet high in vegetables discourages loss Head trauma The 10 Warning Signs 1. Memory loss that disrupts daily life 2. Challenges in planning and problem solving 3. Difficulty completing familiar tasks 4. Confusion with time or place 5. Trouble understanding visual images and spatial relationships 6. New problems with words in speaking or writing 7. Misplacing things, inability to retrace steps 8. Decreased/poor judgment 9. Withdrawal from work or social activities 10. Mood and personality changes I'm seeing some of those symptoms, but how do I know it's not just normal aging? Typical age-related changes Could be Alzheimer's Disease Making a bad decision every once in a while Poor judgment and decision-

making Missing a monthly payment Forgetting which day it is, but remembering later Sometimes forgetting which word to use Losing things from time to time

Inability to manage a budget Losing track of date or season Difficulty holding a conversation Misplacing things and being unable to retrace steps

Sooooooo... If you or a loved one are having experiences such as those above, and especially if they are high-risk, it's time to see the PRIMARY CARE PHYSICIAN-PCP. That's who usually diagnoses AD. Diagnosis The Dr will perform a family history, psychiatric history, history of cognitive and behavioral changes. Ideally, close family members will be involved Cognitive tests, physical and neurological examinations MRI to identify brain changes Soon biomarkers will be used to diagnose AD- beta-amyloid and tau presence may be tested for in cerebrospinal fluid and blood; other tests that indicate damage to or degeneration of neurons Dementia Dementia is the loss of mental functions -- such as thinking, memory, and reasoning -- that is severe enough to interfere with a person's daily functioning. Dementia is not a disease itself, but rather a group of symptoms that are caused by various diseases or conditions that result in damaged neurons and or connections between neurons. DSM-IV Criteria for Dementia *Symptoms must include a decline in memory and in at least one of the following cognitive abilities: Ability to generate coherent speech or understand spoken or written language Ability to recognize objects, assuming intact sensory function Ability to execute motor activities, assuming intact motor abilities, sensory function, and comprehension of the required task, AND Ability to think abstractly, make sound judgements, and plan and carry out complex tasks.

*The decline must be severe enough to interfere with ADLs. THEN Dr. should determine the cause of dementia. Some causes of dementia are treatable: Depression Delirium Drug interaction Thyroid problems Alcoholism Vitamin deficiencies

If the patient isn't experiencing a treatable condition, they should be examined for symptom patterns and distinguishing microscopic brain abnormalities that can help differentiate different types of dementia. There are over 50 types of dementia Such as : Vascular dementia - stroke- symptoms often overlap, but memory may not be as affected -Mixed Dementia- may be AD and another type -Dementia with Lewy Bodies, Parkinson's Disease, frontotemporal dementia, CreutzfeldJakob disease, normal pressure hydrocephalus Alzheimer's Disease is the most common type of dementia, 60%-80% of all cases -According to long-term observational studies, many people with dementia have brain abnormalities associated with more than one type of dementia. New staging guidelines take effect this year: 1. 2. 3. 4. Preclinical Stage: begins as many as 20 years before any symptoms appear. -additional biomarker research is needed, but it hopefully will be able to diagnose measurable changes in CSF and the brain at this phase. Mild cognitive impairment due to AD: mild but measurable changes in thinking abilities, but have no effect on person's ability to carry out every day activities. Dementia due to AD: DSM IV guidelines

The old stages were mild, moderate, and severe, and based on scores on mental-functioning tests that assess memory, awareness of time and place, thinking, and reasoning. Treatment No treatment will alter the underlying course of the terminal disease. FDA has approved 5 drugs that temporarily improve symptoms, but no treatment is available to slow or stop AD.

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Cholinesterase Inhibitors: AD decreases acetylcholine levels in the brain, and we all know ach is important for alertness, memory, thought, and judgment. Dwindling neurons eventually stop being able to produce ach, and these drugs will lose effectiveness. All cholinesterase inhibitors, on average, work about equally well. But in individuals, one cholinesterase inhibitor may work better or produce fewer side effects than does another. They're indicated for different stages of the disease - Donepezil (Aricept), rivastigmine (Exelon), and tacrine (Cognex), and galantamine (Razadyne). Cognex was the first approved, but it's associated with more serious side effects than the other three drugs in this class. All may cause stomach upset, diarrhea, vomiting, muscle cramps, and fatigue.

Memantine (Namenda). For later stages of the disease. Possible side effects include agitation or anxiety. Other Treatment Other meds may be used to control aggressive, agitated, or dangerous behaviors. They are usually given in very low doses to curb risks of side effects and death. Medications that make confusion worse may need to be discontinued. -painkillers, cns depressants, antihistamines, sleeping pills, others Expectations How quickly AD gets worse is different for each person. If AD develops quickly, it is more likely to worsen quickly. Patients with AD often die earlier than normal, although a patient may live anywhere from 3 - 20 years after diagnosis. The final phase of the disease may last from a few months to several years. During that time, the patient becomes totally disabled. Death usually occurs from an infection or organ failure. Prevention Three forms of prevention exist. Primary prevention aims at reducing disease incidence. Secondary prevention aims at preventing preclinical disease from progressing to clinical disease and depends on effective screening and early detection of dementia. Tertiary prevention is geared towards reducing disability, comorbidity, and further disease progression. If effective treatments exist, early detection can lead to modification of dementia risk. Primary: Same preventative measures for cardiovascular health promotion. (exercise, cutting cholesterol, omega 3 fatty acids 2-3x a week, antioxidant-rich diet, NSAID therapy) Maintain social interactions throughout life Stay mentally active Some studies have found correlation between moderate red wine consumption and 50% lower incidence of disease Vaccine in research stage:

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An accomplice to the protein that causes plaque buildup in Alzheimers disease is the focus of a potential new treatment, according to research by a Georgia Health Sciences University graduate student. In Alzheimers, the amyloid protein can accumulate in the brain instead of being eliminated by the bodys natural defenses, nestling between the neurons and forming impassable plaques. Amyloid and the way it gets there could be targets for a new vaccine. RAGE, or receptor for advanced glycation endproducts, proteins bind to amyloid and transport it into the brain, said Scott Webster, a fifth-year graduate student who is studying the disease in the lab of Dr. Alvin Terry, Professor of Pharmacology and Toxicology. Research has shown that RAGE may also contribute to the inflammation and damage that amyloid causes to the brains nerve cells. Early results have shown improved cognition and memory in animal models of Alzheimers.

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