Final answer:
In Alzheimer's disease, the affected nerve cells in the brain accumulate neurofibrillary tangles and amyloid-beta plaques, leading to neuron dysfunction and death, particularly severe in the hippocampus, impacting memory and cognition.
Step-by-step explanation:
In Alzheimer's disease, affected nerve cells in the brain are filled with abnormal collections of twisted protein threads called neurofibrillary tangles and deposits of apparently toxic protein fragments called amyloid-beta plaques.
Alzheimer's disease, named after Alois Alzheimer, a German psychiatrist, is characterized by the accumulation of amyloid-beta plaques between brain cells and neurofibrillary tangles within the neurons. These accumulations are toxic to the neurons, leading to impaired neuronal function, loss of connections, and ultimately neuronal death. Especially in the hippocampus, the loss of neurons can be severe, which impacts memory and cognitive functions. These findings are common in both familial and sporadic cases of Alzheimer's disease. Moreover, research suggests that altered protein conformations may contribute to disease pathologies, as misfolded proteins become toxic. In Alzheimer's, specifically, the amyloid beta peptide derived from the enzymatic cleavage of the amyloid precursor protein forms these plaques, while hyperphosphorylated tau protein forms neurofibrillary tangles.