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Alzheimer's Disease Pathology
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Alzheimer's Disease (AD) is the most common form of dementia and is characterized by progressive neurodegenerative changes that impair cognitive functions and daily living activities. The pathology of Alzheimer's is marked by distinctive changes in the brain, notably the accumulation of amyloid-beta plaques and neurofibrillary tangles.
Key Pathological Features:
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Amyloid-beta Plaques: These are extracellular deposits primarily composed of amyloid-beta peptide, a protein fragment derived from the amyloid precursor protein (APP). These plaques accumulate in the brain tissue, disrupting cell-to-cell communication and triggering inflammatory responses that damage neurons.
Neurofibrillary Tangles: These are intracellular accumulations of hyperphosphorylated tau protein. Tau normally helps stabilize microtubules in neurons; however, in AD, tau proteins become abnormally twisted and tangled, leading to the collapse of the neuron's transport system.
Neuronal Loss and Brain Atrophy: As AD progresses, there is a significant loss of neurons and synapses, particularly in the hippocampus and cortex, which are crucial for memory and cognition. This neuronal loss results in gross atrophy of the affected regions of the brain, visible on MRI and other imaging techniques.
Neurochemical Changes: There is a marked decline in the levels of key neurotransmitters, including acetylcholine, which is crucial for learning and memory processes. This decline is associated with the severity of cognitive symptoms.
Chronic Inflammation: Chronic inflammation plays a critical role in the progression of Alzheimer's. Microglial cells, the brain's immune cells, become activated and may exacerbate neuronal damage by releasing inflammatory mediators.
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Негізгі бет 7. Alzheimer's Disease Pathology : USMLE Step 1
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