* Blocking the metabotropic glutamate receptor 5 protein may repair memory
* Tests have shown that it restores learning in mouse model of Alzheimer's
* Findings could help develop drugs to slow the degenerative illness
4 September 2013
Researchers have discovered a protein that they claim is the missing link to the development of Alzheimer's disease.
They found that blocking this protein with an existing drug can restore memory in mice with brain damage that mimics the disease.
The findings could offer hope of developing drugs to slow the degenerative illness.
Alzheimer's causes a decrease in the size of the brain, shown here by the enlarged ventricle cavities (white, at centre of brain) and the widened pale blue regions. Researchers now believe they have found the 'missing link' that triggers the disease
'What is very exciting is that of all the links in this molecular chain, this is the protein that may be most easily targeted by drugs,' said the study's senior author Stephen Strittmatter at Yale School of Medicine.
'This gives us strong hope that we can find a drug that will work to lessen the burden of Alzheimer's.'
During Alzheimer's disease protein 'plaques' develop in the structure of the brain, leading to the death of brain cells.
People with Alzheimer's also have a shortage of some important chemicals in their brain involved with the transmission of messages within the brain.
Scientists have already provided a partial molecular map of how Alzheimer's disease destroys brain cells.
In earlier work, Professor Strittmatter's lab showed that the amyloid-beta peptides, which are a hallmark of Alzheimer's, couple with prion proteins.
By an unknown process, the coupling activates a molecular messenger called Fyn.The new findings, published in the journal Neuron, reveals the missing link in the chain, a protein within the cell membrane called metabotropic glutamate receptor 5, or mGluR5.
When the protein is blocked by a drug similar to one being developed for Fragile X syndrome, the deficits in memory, learning, and synapse density were restored in a mouse model of Alzheimer's.
Prof Strittmatter stressed that new drugs may have to be designed to precisely target the amyloid-prion disruption of mGluR5 in human cases of Alzheimer's and said his lab is exploring new ways to achieve this.
Alzheimer's disease is the most common cause of dementia, currently affecting around 496,000 people in the UK.