London, July 1 (IANS) Elevated activity in the hippocampus – the area of the brain that controls learning and memory – is linked with mild cognitive impairment and early stages of Alzheimer’s disease.
Researchers have now discovered the molecular mechanism that may trigger an enhancement of neuronal activity in Alzheimer’s patients, which subsequently damages memory and learning functions.
The amyloid precursor protein (APP), in addition to its well-known role in producing a protein fragment known as amyloid-beta, also constitutes the receptor for amyloid-beta.
The binding of amyloid-beta to pairs of APP molecules triggers a signalling cascade, which causes elevated neuronal activity, the study said.
“Our work suggests that APP molecules, like many other known cell surface receptors, may modulate the transfer of information between neurons,” said Inna Slutsky from Tel Aviv University in Israel.
Hyperactive hippocampal neurons, which precede amyloid plaque formation, have also been observed in mouse models with early onset Alzheimer’s disease.
The research project was launched five years ago, following the researchers’ discovery of the physiological role played by amyloid-beta, previously known as an exclusively toxic molecule.
The team found that amyloid-beta is essential for the normal day-to-day transfer of information through the nerve cell networks.
If the level of amyloid-beta is even slightly increased, it causes neuronal hyperactivity and greatly impairs the effective transfer of information between neurons.
While unaffected “normal” neurons became hyperactive following a rise in amyloid-beta concentration, neurons lacking APP did not respond to amyloid-beta.
“This finding was the starting point of a long journey toward decoding the mechanism of APP-mediated hyperactivity,” Slutsky noted.
The findings appeared in the journal Cell Reports.
