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Discuss the clinical progression of Alzheimer's disease symptoms.
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Symptoms evolve from undetectable to short-term memory loss, language difficulty, motor skill loss, long-term memory issues, and eventually a pervasive bedridden state with infection risks.
What are the observable changes in brain structure due to Alzheimer’s disease?
Alzheimer's causes brain atrophy, characterized by narrowed gyri, widened sulci, and enlarged ventricles due to neuron death.
What genetic factors are associated with increased Alzheimer’s disease risk?
Genetic factors include the APOE E4 allele for sporadic forms and mutations in PSEN1 and PSEN2 genes for familial early-onset forms.
What is the significance of trisomy 21 in Alzheimer's disease?
Trisomy 21, or Down syndrome, leads to increased APP production due to an extra chromosome 21, heightening amyloid plaque buildup and Alzheimer's risk.
How do neurofibrillary tangles form and affect neurons?
Tau proteins destabilize as amyloid plaques activate kinase, causing tangles that impair intracellular support and neuron signaling, often leading to apoptosis.
What is the role of amyloid precursor protein (APP) in Alzheimer's disease?
APP is crucial for neuron growth and repair. When APP is cleaved incorrectly by beta secretase, it leads to the formation of amyloid beta monomers that cluster into beta amyloid plaques.
Describe the impact of tau protein alteration in Alzheimer's disease.
Once tau proteins are altered by plaque-induced kinase activation, they form tangles that disrupt microtubule stability, leading to neuron dysfunction and death.
Why is diagnosing Alzheimer's disease challenging?
Definitive diagnosis requires a brain biopsy post-autopsy; typically diagnosed by excluding other types of dementia.
How do amyloid plaques contribute to amyloid angiopathy?
Plaques weaken blood vessel walls, making them more susceptible to hemorrhage, which can exacerbate cognitive impairment.
What limitations exist in current Alzheimer’s treatments?
Current treatments offer minimal benefits, failing to cure or significantly halt disease progression.
Differentiate between sporadic and familial Alzheimer's disease.
Sporadic Alzheimer's is typically late-onset with unclear causes and age influence, while familial Alzheimer's is early-onset, inherited, linked to gene mutations (e.g., PSEN1, PSEN2).
Explain how amyloid beta plaques affect neuronal function.
Plaques disrupt neuron signaling, impair memory, trigger immune responses leading to inflammation, potential damage to neurons, and increase hemorrhage risk through amyloid angiopathy.
How does the APOE E4 allele influence the risk of developing Alzheimer's?
The APOE E4 allele is associated with higher Alzheimer's risk, with one or two alleles significantly increasing likelihood.
What is dementia and what are its primary causes?
Dementia is a set of symptoms affecting memory, learning, and independent functioning, usually caused by damage to brain cells from various diseases.
Describe the pathophysiological changes in the brain associated with Alzheimer's disease.
Alzheimer's disease features neurodegeneration due to beta amyloid plaques and neurofibrillary tangles, leading to disrupted neuron signaling, inflammation, and brain atrophy.
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