Researchers have discovered that the genetic mechanism which destroys brain cells is responsible for early development of Alzheimer's Disease in people with Down Syndrome and for development of Alzheimer's Disease in general population.
This discovery by researchers at the University of British Columbia and Vancouver Coastal Health Research Institute provides a potential new target for drugs that could forestall dementia in people with either condition.
AdvertisementThe research, led by Dr. Weihong Song, Canada Research Chair in Alzheimer's Disease and a professor of psychiatry in the UBC Faculty of Medicine, found that excessive production of a protein, called Regulator of Calcineurin 1 (RCAN1), sets in motion a chain reaction that kills neurons in the hippocampus and cortex in people with Down Syndrome (DS) and Alzheimer's Disease (AD).
"Neuronal death is the primary reason for the memory loss and other cognitive impairments of Alzheimer's Disease, and it's the main reason people with Down Syndrome develop Alzheimer's Disease long before most people, usually in their 30s," said Song, a member of the Brain Research Centre at UBC and the Vancouver Coastal Health Research Institute (VCHRI), and Director of Townsend Family Laboratories at UBC.
People with DS have an extra copy of the gene that produces RCAN1, thus leading to its excess production. The resulting neuronal death - with symptoms that mirror those of AD patients - is one of the prime reasons for the shortened lifespan of people with DS.
The research team discovered that some AD patients have similarly elevated levels of the RCAN1 protein, despite having two copies of the responsible gene. It's still unknown why, though Song speculates that the gene's overexpression might be triggered by stroke, hypertension or the presence of a neurotoxic protein, called beta amyloid, that typically collects into clumps in the brains of people with AD - what he describes as a "vicious cycle" in which one destructive factor exacerbates another.
The findings have been published online in the Journal of Biological Chemistry.
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