Another Genetic Cause Of Alzheimer's Disease

Another Genetic Cause Of Alzheimer's Disease.
Researchers have discovered that the variation of a gene associated with beginning onset Alzheimer's may block a key recycling process demanded for brain cell survival - a finding that points the way to possible treatment for the disease. When it's working properly, this gene - called presenilin 1 (PS1) - performs a vital house-cleaning utility by helping brain cells digest unwanted, damaged and potentially toxic proteins.

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

And "Presently, no effective treatment exists to either unproductive 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 unearthing has the the of identifying such a treatment".

Mutations of the PS1 gene have previously been thought to broaden 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 doltish or balk Alzheimer's progression.

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

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