Another Genetic Cause Of Alzheimer's Disease

Another Genetic Cause Of Alzheimer's Disease.

Researchers have discovered that the metamorphosing of a gene associated with advanced onset Alzheimer's may block a key recycling process life-and-death for brain cell survival - a finding that points the way to possible treatment for the disease as an example. When it's working properly, this gene - called presenilin 1 (PS1) - performs a essential house-cleaning putting into play by helping brain cells digest unwanted, damaged and potentially toxic proteins.

But in its mutated form, the gene fails to employee cells recycle these dormant toxins, suggesting an explanation for the damage to the brain characteristic of Alzheimer's disease more. "We find creditable we have identified the principal mechanism by which mutations of PS1 cause the most common genetic type of Alzheimer's disease," study co-author Dr Ralph A Nixon, professor in the departments of psychiatry and stall biology as well as director of NYU's Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute, said in a university intelligence release.

And "Presently, no effective treatment exists to either reluctant or prevent the progression of Alzheimer's disease," added Nixon, also director of the Center for Dementia Research at the Nathan S Kline Institute for Psychiatric Research in New York City. "This invention has the possibility of identifying such a treatment".

Mutations of the PS1 gene have previously been thought to prolong production of the toxic beta amyloid protein that appears to collect in the brains of Alzheimer's patients. In turn, scientists have theorized that by preventing amyloid deposits from accumulating, they might be able to humdrum or delay Alzheimer's progression.

However, the current investigation into PS1 behavior side-steps this potential scenario - without questioning its validity - by focusing on the plausibility that abnormal PS1 function may cause cell extermination unconnected to beta amyloid buildup. PS1 mutations and other factors could, therefore, patronize Alzheimer's in entirely different ways, the team said.

So "There is an urgent need now to appreciate Alzheimer's disease as caused by multiple factors and approach the treatment from that perspective," said Nixon, who added that the accepted finding opens up a new target for Alzheimer's interventions down the road. Focusing on how to rejuvenate brain cells' normal recycling system is a promising therapeutic approach since its disruption appears to present Alzheimer's homepage. Nixon and his colleagues report their findings in the June 10th online efflux of the journal Cell.

tag : alzheimer disease brain treatment nixon amyloid cells mutations approach



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