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MIT IDs enzymes key to brainpower
November 7, 2007
Bolstering disintegrating neural connections may help boost brainpower in
Alzheimer's disease patients, MIT researchers and colleagues will report in the
Nov. 8 issue of Neuron.
The researchers zeroed in on the enzymes that manipulate a key scaffolding
protein for synapses, the connections through which brain cells communicate.
Synapses are weakened and lost in neurodegenerative diseases such as Alzheimer's
and Parkinson's disease.
"We identified a major underlying mechanism through which synapses are
strengthened and maintained," said Morgan H. Sheng, Menicon Professor of
Neuroscience at MIT's Picower Institute for Learning and Memory. "The enzymes
involved could be good targets for potential drug treatments."
A protein called postsynaptic density-95 (PSD-95) is a key building block of
synapses. Like the steel girders in a building, it acts as a scaffold around
which other components are assembled. "The more PSD-95 molecules, the bigger and
stronger the synapse," said co-author Myung Jong Kim, a Picower research
scientist.
Previous research had shown that mice genetically altered to have less PSD-95
experienced learning and memory problems.
In the current study, the researchers identified for the first time the enzymes
that work behind the scenes on PSD-95, adding a phosphate group to a specific
amino acid in the PSD-95 protein. This process--called phosphorylation--is
critical for PSD-95 to do its job in supporting synapses.
"Adding a phosphate group to a single amino acid allows PSD-95 to promote
synapse size and strength," said Sheng, who also holds an appointment in MIT's
Department of Brain and Cognitive Sciences and is a Howard Hughes Medical
Institute investigator. "Therefore, promoting this process could help improve
cognitive function."
Sheng believes manipulating PSD-95 through phosphorylation could lead to bigger
and more robust synapses, which would boost brainpower in both normal and
diseased brains. "It's possible that promoting PSD-95 phosphorylation could also
help neuropsychiatric illnesses in which synapse function goes awry, such as
schizophrenia, depression and autism," Sheng said.
In addition to Sheng and Kim, authors include Picower research scientist Kensuke
Futai; Yasunori Hayashi, MIT assistant professor of neurobiology and RIKEN-MIT
investigator; and Jihoon Yu and Kwangwook Cho of the University of Bristol in
England.
This research is supported by the National Institutes of Health.
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