0000000000447085
AUTHOR
Viviana Culmone
Progressive effect of beta amyloid peptides accumulation on CA1 pyramidal neurons: a model study suggesting possible treatments
Several independent studies show that accumulation of β-amyloid (Aβ) peptides, one of the characteristic hallmark of Alzheimer's Disease (AD), can affect normal neuronal activity in different ways. However, in spite of intense experimental work to explain the possible underlying mechanisms of action, a comprehensive and congruent understanding is still lacking. Part of the problem might be the opposite ways in which Aβ have been experimentally found to affect the normal activity of a neuron; for example, making a neuron more excitable (by reducing the A- or DR-type K(+) currents) or less excitable (by reducing synaptic transmission and Na(+) current). The overall picture is therefore confus…
A model study for the progressive disruption of CA1 firing properties during Alzheimer’s disease
Several independent studies show that β-Amyloid (Aβ) peptides accumulation, one of the characteristic hallmark of Alzheimer’s Disease (AD), can affect the normal neuronal activity in different ways causing an increase or a decrease in neuronal membrane excitability. For example, experimental evidence for a negative impact on neuronal membrane in animal models of AD has been obtained in dual patch recordings in rat hippocampal tissue slices, in which Aβ blocked K channels in pyramidal cell dendrites, causing an increase in dendritic membrane excitability. The resulting increased Ca2+ influx and excitoxicity may lead to dendritic degeneration. However, further experimental evidence suggests t…