Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia
Posted Dec 29 2011 9:02pm
A recent paper on Down Syndrome and dementia shows some similarities to some recent trends in autism research. Beyond that, it points out the type of knowledge that is missing about autistic adults. The type of research which begs the question of why there is relatively little effort ongoing into autistic adults.
People with Down syndrome, also called trisomy 21, develop a syndrome of dementia that has the same characteristics of Alzheimer’s disease that occurs in individuals without Down syndrome. The only difference is that Alzheimer’s disease occurs much earlier in people with Down syndrome; patients with Down syndrome begin to have symptoms in their late 40s or early 50s.
Most (and maybe all) people with Down syndrome develop the brain changes associated with Alzheimer’s disease. However, Alzheimer’s disease is not more common in individuals with intellectual disabilities from causes other than Down syndrome. An estimated 10%-25% of patients with Down syndrome have Alzheimer’s disease at age 40-49 years, 20%-50% have Alzheimer’s disease at age 50-59 years, and 60%-75% have Alzheimer’s disease when older than 60 years of age. Alzheimer’s disease decreases survival in people with Down syndrome who are older than 45 years of age.
Much effort and discussion goes into the question of medical concerns in autistic children (for example, gastro-intestinal complaints). Are there any medical concerns which are more common in autistic adults than in the general population? There are two ways to find out. (1) Identify and study autistic adults now. (2) Wait 50 years or so for this generation of children to age. It would seem clear that (2) would be the less desirable choice.
Here is the abstract for the paper, Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia:
Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia.
Perluigi M, Butterfield DA.
Department of Biochemical Sciences, Faculty of Pharmacy and Medicine, Sapienza University of Rome 00185 Rome, Italy.
Down syndrome (DS) is one of the most frequent genetic abnormalities characterized by multiple pathological phenotypes. Indeed, currently life expectancy and quality of life for DS patients have improved, although with increasing age pathological dysfunctions are exacerbated and intellectual disability may lead to the development of Alzheimer’s type dementia (AD). The neuropathology of DS is complex and includes the development of AD by middle age, altered free radical metabolism, and impaired mitochondrial function, both of which contribute to neuronal degeneration. Understanding the molecular basis that drives the development of AD is an intense field of research. Our laboratories are interested in understanding the role of oxidative stress as link between DS and AD. This review examines the current literature that showed oxidative damage in DS by identifying putative molecular pathways that play a central role in the neurodegenerative processes. In addition, considering the role of mitochondrial dysfunction in neurodegenerative phenomena, results demonstrating the involvement of impaired mitochondria in DS pathology could contribute a direct link between normal aging and development of AD-like dementia in DS patients.