Final answer:
Alzheimer's disease features protein aggregation manifesting as amyloid plaques and tau protein tangles, leading to the loss of neurons and cognitive abilities. It starts in the hippocampus and is considered a 'proteopathy', with potential treatments targeting protein misfolding and aggregation.
Step-by-step explanation:
Understanding Alzheimer's Disease and Protein Aggregation
Alzheimer's disease is a degenerative brain disorder characterized by the accumulation of amyloid plaques and tau protein tangles. These pathological features contribute to the progressive deterioration of neurons, leading to symptoms such as memory loss and dementia. The formation of amyloid plaques involves the misfolding of amyloid beta (Aß) proteins from α-helix to ß-pleated sheets, which then aggregate. Abnormal tau proteins accumulate inside neurons, forming neurofibrillary tangles that disrupt neuronal function and connectivity, especially in the hippocampus, where the disease typically begins. Research is ongoing to understand the exact mechanisms involved, including the roles of excitotoxicity and synaptic loss, contributing to the cognitive decline observed in Alzheimer's patients.
Protein misfolding diseases like Alzheimer's are categorized as 'proteopathies', where functional proteins assume toxic conformations and aggregate. This discovery has opened new therapeutic possibilities, aiming to disrupt protein accumulation or address its production. As Alzheimer's is a complex and multifactorial disease, understanding and targeting these processes could be key in slowing down or preventing the disease progression.