Potential Alzheimer's breakthrough !!!
- Summary:
- A New Gene and associated protein (which they have named 'Aggregatin') could potentially be suppressed to slow the advance of Alzheimer's disease.
FULL STORY
A new gene and associated protein which could potentially be
suppressed to slow the advance of Alzheimer's disease has been identified !
"This protein can be a new
risk factor for Alzheimer's disease (AD),"
"We also see this as a potential novel therapeutic target for this devastating disease."
Wang said proving the latter assertion, which has not yet been tested in humans, would require additional research to corroborate the function of the protein they have dubbed "aggregatin." Eventually, that would someday mean clinical trials with Alzheimer's patients, he said.
"This protein characteristically accumulates, or aggregates, within the center of plaque in AD patients, like the yolk of an egg -- which is part of the reason we named it "aggregatin,"
A patent has been filed for "novel Alzheimer's disease treatments and diagnosis based on this and related study,"
"This is probably the first systematic work combining the identification from a genome-wide association study of high dimensional brain-imaging data and experimental validation so perfectly in Alzheimer's disease,"
The role of 'aggregatin' protein
Researchers began by correlating roughly a million genetic markers (called single-nucleotide polymorphisms, or SNPs) with brain images. They were able to identify a specific SNP in the FAM222, a gene linked to different patterns of regional brain atrophy.
The protein encoded by gene FAM222A is not only associated with AD patient-related beta-amyloid plaques and regional brain atrophy, but that "aggregatin" attaches to amyloid beta peptide -- the major component of plaque and facilitates the plaque formation.
So when researchers injected mouse models with the "aggregatin" protein (made from the FAM222A gene), plaque (amyloid deposits) formation accelerated in the brain, resulting in more neuroinflammation and cognitive dysfunction. This happened, they report, because the protein was found to bind directly the amyloid beta peptide, thus facilitating the aggregation and placque formation, Wang said.
Conversely, when they suppressed the protein, the plaques were reduced and neuroinflammation and cognitive impairment alleviated.
Reducing levels of this protein and inhibition of its interaction with amyloid beta peptide could potentially be therapeutic -- not necessarily to prevent Alzheimer's but to slow its progression.
"We also see this as a potential novel therapeutic target for this devastating disease."
Wang said proving the latter assertion, which has not yet been tested in humans, would require additional research to corroborate the function of the protein they have dubbed "aggregatin." Eventually, that would someday mean clinical trials with Alzheimer's patients, he said.
"This protein characteristically accumulates, or aggregates, within the center of plaque in AD patients, like the yolk of an egg -- which is part of the reason we named it "aggregatin,"
A patent has been filed for "novel Alzheimer's disease treatments and diagnosis based on this and related study,"
"This is probably the first systematic work combining the identification from a genome-wide association study of high dimensional brain-imaging data and experimental validation so perfectly in Alzheimer's disease,"
The role of 'aggregatin' protein
Researchers began by correlating roughly a million genetic markers (called single-nucleotide polymorphisms, or SNPs) with brain images. They were able to identify a specific SNP in the FAM222, a gene linked to different patterns of regional brain atrophy.
The protein encoded by gene FAM222A is not only associated with AD patient-related beta-amyloid plaques and regional brain atrophy, but that "aggregatin" attaches to amyloid beta peptide -- the major component of plaque and facilitates the plaque formation.
So when researchers injected mouse models with the "aggregatin" protein (made from the FAM222A gene), plaque (amyloid deposits) formation accelerated in the brain, resulting in more neuroinflammation and cognitive dysfunction. This happened, they report, because the protein was found to bind directly the amyloid beta peptide, thus facilitating the aggregation and placque formation, Wang said.
Conversely, when they suppressed the protein, the plaques were reduced and neuroinflammation and cognitive impairment alleviated.
Reducing levels of this protein and inhibition of its interaction with amyloid beta peptide could potentially be therapeutic -- not necessarily to prevent Alzheimer's but to slow its progression.
Source:
Materials provided by Case Western Reserve University. Note: Content may be edited for style and length.
https://www.sciencedaily.com/releases/2020/01/200122080532.htm
Their research was published this month by the scientific journal Nature Communications and supported by grants from the National Institutes of Health (NIH) and the Alzheimer's Association. Genomic and brain imaging data was obtained from the Alzheimer's Disease Neuroimaging Initiative, which is supported by the NIH.
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