Alzheimers Disease

605 Week 1 Advanced PathophysConcept Map

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Alzheimers Disease by Mind Map: Alzheimers Disease

1. Pathophysiology: Neurocognitive disorder with progress cognitive deterioration, characterized by beta-amyloid deposits and neurofibrillary tangles in the cerebral cortex and subcortical gray matter

2. Etiology: Progressive deterioration in function from neurotransmitter deficiency; prevalent form of dementia is characterized by memory loss, deficits in thought process and behavioral changes

3. Treatment Medications: Eg. Memantine, Cholinesterase Inhibitors - Cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) increase cholinergic transmission by inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia. Antioxidants: Vitamin E, Selegiline Nonpharmacologic Therapy and Supportive Care: Behavioral disturbance, nutrition, Rehab (cognitive rehab, exercise programs, OT) Risk factor Control Alcohol Safety/societal issues

4. Risk Factors: Advanced age (1 in 26 people at age 65; 2 in 5 after age 85), female gender, head trauma, Genetics: family history Genetic risk factors AD family history of dementia, rare dominantly inherited mutations in genes that impact amyloid in the brain, and the apolipoprotein E (APOE) epsilon 4 (e4) allele. Early-onset AD -autosomal dominant inheritance pattern related to mutations in genes that alter amyloid beta protein production, aggregation, or clearance, including amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2). highly penetrant, meaning that carriers have a nearly 100 percent chance of developing the disease in their [email protected] 65 Late Onset -genetic risk factor for late-onset AD is APOE; carriers of one e4 allele are at two- to threefold increased odds of developing AD compared with noncarriers, and those with two e4 alleles are at approximately 8- to 12-fold increased odds. -strength of the association may be modified by several factors, including gender, race, and vascular risk factors

5. Diagnostic Tests: Genetic testing/Histopathologic examination for APP, PSEN1, and PSEN2 mutations Neuropsychologic testing Neuroimaging Laboratory tests/Biomarkers

6. Common Findings: Clinical assessment AD should be suspected in any older adult with insidious onset, progressive decline in memory, and at least one other cognitive domain leading to impaired functioning. - Cardinal symptoms: Memory impairment, decline in executive function and judgement/problem solving -detailed cognitive and general neurologic examination