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Alzheimers Disease


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Definition, etiolog, clinical manifestations, pathophysiology and diagnosis of Alzheimers disease

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Alzheimers Disease

  1. 1. 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. AD is also known as senile dementia of the Alzheimer type (SDAT) or simply Alzheimer's the most common form of dementia. It is an incurable, degenerative, terminal disease. AD results from an increase in the production or accumulation of specific protein (β-amyloid protein) in the brain that leads to nerve cell death
  2. 2. • • The exact etiology of Alzheimer’s disease is unknown and associated with risk factors But stated that there are several GENETICAL and ENVIRONMENTAL factors have been explored as potential causes of the Alzheimer’s disease
  3. 3. RISK FACTOR for developing the Alzheimer's disease • • • • • Increased age (over 65 years of age) Hypertension (high blood pressure) Increased cholesterol levels Coronary artery disease Diabetes OTHER risk factors are • • • • • Genetics Smoking and alcohol use Plasma homocysteine Down syndrome Mild cognitive impairment
  4. 4.  There are two signature lesions in Alzheimer’s Disease. They are 1. Neuritic Plaques: Deposits of β- amyloid protein that accumulates in the spaces between the nerve cells. 2. Neurofibrillary Tangles (NFT’s): Deposits of the protein tau that accumulates inside the nerve cells
  5. 5. Cleared by β-secretase -secretase  secretase has two genes 1 & 2, When these undergoes mutation They lead to increased cleaving of  secretase. These sed cleaving of APP results in increased production of β- amyloid protein mutation of amyloid precursor protein on chromosome no 21 increased production of amyloid precursor protein Produces of amyloid protein Accumulation of β amyloid protein (due to increased production of APP) Directly neurotoxin Alzheimer’s disease
  6. 6.   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.
  7. 7. SYMPTOMS COGNITIVE: • Memory loss • Aphasia • Apraxia • Agnosia • Disorientation • Impaired executive function NON COGNITIVE • Depression, psychotic symptoms(hallucination and delusions) • Behavioral disturbances(physical and verbal aggression, motor hyperactivity, uncooperativeness, wandering, repetitive mannerisms and activities, and combativeness) FUCTIONAL • Inability to care for self (dressing, bathing, toileting, and eating)
  8. 8. EARLY MILD MODERATE SEVERE DURATION: 2-4 years SYMPTOMS: • Recent memory loss • Repeated questions • Problems with language • Depression • Apathy • Personality changes • Need reminders for daily activities 2-10 years • Persistent memory loss • Rambling speech • Unusual reasoning • Confusion • Sleep disturbance • Mood & behavioral changes • Slowness • Rigidity • Tremors • Gait --- • Increased memory loss and confusion • Inability to learn things • Delusions • Paranoia • Problems recognizing family and friends 1-3 years • Total loss of verbal skills • Unable to care for self • Falls possible and immobiling likely • Problems with swallowing • Incontinence and illness • Hallucinations and delusions • Patient needs total care and support
  9. 9.  Detailed patient history  Information from family and friends  Laboratory tests like • Rule out vitamin B12 and folate deficiency • Rule out hypothyroidism with TFT tests Blood cell count, serum electrolytes, LFT •  Other diagnostic tests • CT,PET or MRI scans may aid diagnosis
  10. 10.   Principle of Pharmacotherapeutics by Joseph.Dipiro Textbook of Pathophysiology by Harsh Mohan