Dementia Today.net

Site updated at Wednesday, 22 June 2016

Living with Dementia

Alzheimer’s disease works differently in patients with and without Down syndrome

  • - Dementia News
  • Jun 26, 2015
  • Comments
  • Viewed: 0
Tags: | alzheimer's disease | amyloid precursor protein | down syndrome |

Researchers at the University of Kentucky’s Sanders-Brown Center on Aging have completed a study that revealed differences in the way brain inflammation - considered a key component of AD—is expressed in different subsets of patients, in particular people with Down syndrome (DS) and AD.

People with Down syndrome have a third copy of Chromosome 21, and that chromosome is the same one responsible for the production of a molecule called amyloid precursor protein. Amyloid overproduction can lead to brain plaques that are a cardinal feature of Alzheimer’s, so it is not surprising that nearly 100 percent of people with Down syndrome develop Alzheimer’s disease pathology in their brain by the time they are 40.

People develop Alzheimer’s disease at different ages, but it’s typically in their 60s, 70s, or 80s,” said Donna Wilcock, an assistant professor at the Sanders-Brown Center on Aging and principal investigator for the study. “It’s a little easier to study Alzheimer’s disease in Down syndrome because of the predictability of the age when adults with DS develop signs of the disease.”

In Wilcock’s study, some interesting data emerged that will shape the way scientists look at AD as manifested in various subsets of the population. Using brain autopsy tissue from a group of people—some with DS/AD, some with AD alone, and some healthy, Wilcock and her team were able to determine differences in the way neuroinflammation was expressed in people with DS.

In previous studies where Wilcock and her colleagues identified different types of inflammation in AD brains,, two families of inflammatory markers - called M1 and M2a - were each present to varying degrees in the sample population representing early AD cases, indicating a notable level of heterogeneity in the way the AD disease process begins in the brain. But in the late-stage AD cases, there was a high degree of homogeneity with high levels of the markers M1, M2 and M2c.

If you think of it in terms of a roadmap, there is almost always more than one way to get from Point A to Point B, and that seems to be the case in disease progression as well,” said Wilcock.

In this most recent study, the team found that the inflammatory response in DS/AD brain tissue was significantly greater than that in tissue from AD patients. Further, there was an elevated level of markers for M2b,that was not replicated in tissue from sporadic (i.e. ideopathic) AD cases.. In other words, AD in the DS brain had a very different neuroinflammatory profile than AD in people without DS.

“It has been generally assumed that AD presents the same way in people with Down syndrome as it does in people without DS, but our work demonstrates that this is not the case,” said Wilcock. “This will have important implications for the study of AD treatments, as some treatments might be effective with people without DS but not those with DS, and vice-versa.”

Wilcock’s work has been published online in the Neurobiology of Aging. This study was part of a larger DS Aging study at the Sanders-Brown Center on Aging funded by NIH/NICHD (Head and Schmitt), and was also funded by a research grant awarded to Dr. Wilcock through a partnership between the Alzheimer’s Association, the Global Down Syndrome Foundation and the Linda CRNIC Institute for Down syndrome.

###

The Sanders-Brown Center on Aging is one of the world’s leading research centers on age-related diseases. SBCoA improves the health of the elderly through research, education and outreach programs related to understanding the brain’s aging process and managing age-related cognitive impairment.

###

Laura Dawahare
.(JavaScript must be enabled to view this email address)
859-257-5307

University of Kentucky

Post a comment [ + Comment here + ]

There are no comments for this entry yet. [ + Comment here + ]




Comment
Your details

* Required field


Please enter the word you see in the image below:

Comments are moderated by our editors, so there may be a delay between submission and publication of your comment. Offensive or abusive comments will not be published.

Enid and George - Life with dementia

presbyophrenia1 - university of southern california2 - amyloid-beta peptides1 - cerebrovascular disease1 - gene therapy1 - people with dementia4 - cancer1 - amentia2 - retinopathy1 - korsakoff's syndrome10 - risk factors1 - end-stage dementia1 - ucla1 - tau tangles1 - long-term memory1 - voxel-based morphometry1 - cognitive functions1 - basal ganglia1 - lewy body dementia2 - amyloid-β1 - entorhinal cortex1 - visual hallucinations1 - delirium8 - emotional symptoms1 - delirious episode1 - regular exercise1 - bonfiglio1 - alzheimer's genes1 - cognitive1 - progressive movement disorder2 -