  Alzheimer's disease (AD) is a common form of dementia observed in the elderly
due to neurodegenerative disorder and dysfunction. This arises from alterations
in synaptic functioning of neurons leading to cognitive impairment and memory
loss. Recent experimental studies indicate that the amyloid beta (A beta)
protein, in its dimer and oligomer forms, affects the synaptic activity of
neurons in the early stages of AD. However, the precise mechanism underlying A
beta induced synaptic depression is still not clearly understood. In this
paper, we introduce an electrical model that provides a possible mechanism for
this. Our studies show that the competing effects of synaptic activity and the
indirect interaction mediated by A beta, can disrupt the synchrony among
neurons and severely affect the neuronal activity. This then leads to
sub-threshold activity or synaptic silencing. This is in agreement with the
reported disruption of cortical synaptic integration in the presence of A beta
in transgenic mice. We suggest that direct electrophysiological measurements of
A beta activity can establish its role in AD and the possible revival, proposed
in our model. The mechanism proposed here is quite general and could account
for the role of the relevant protein in other neuronal disorders also.
