The role of amyloid β peptide in synaptic alterations and spine loss

Abstract

Alzheimer’s disease is the most prevalent neurologic disorder, it affects approximately 10 % of the population over the age of 65. Within the population over the age of 85 even more than 50% has AD. The AD brain is characterized by deposits of extracellular neuritic plaques and intracellular neurofibrillary tangles. An important molecule in the development of AD is amyloid β (Aβ). Aβ is formed out of the amyloid precursor protein (APP) and it forms the extracellular neuritic plaques that are detected in AD brains. However, there seems to be no correlation between the amount of neuritic plaques and cognitive deficits. Multiple studies with mouse models indicated that smaller complexes of Aβ, the Aβ oligomers, seems to play an important role in the development of AD. It was shown that Aβ oligomers altered the synaptic signaling and that it induced spine loss.