While it is not yet clear what causes Alzheimer’s disease, researchers are examining a variety of genetic, environmental, and lifestyle causes. New research examines some of the key brain regions involved in the development of Alzheimer’s and finds several fatty acids to be associated with this form of dementia.
The Alzheimer’s Association estimate that every 66 seconds, an adult in the United States develops Alzheimer’s disease (AD). Alzheimer’s-related mortality has increased by as much as 89 percent since the year 2000.
Researchers are hard at work trying to understand what causes AD. It is estimated that the disease affects 1 in 3 older adults in the U.S., and understanding why Alzheimer’s tends to strike seniors, in particular, is at the heart of the medical community’s research efforts.
Researchers are studying late-onset Alzheimer’s in the context of age-related brain changes. A new study – published in the journal PLOS Medicine – looks at how fatty acid metabolites in the brain tissue of healthy seniors behave and affect the participants’ cognitive abilities.
The international research team – led by Cristina Legido-Quigley of King’s College London in the United Kingdom, and Madhav Thambisetty of the National Institute on Aging in the U.S. – conducted a nontargeted metabolite profiling study that analyzed the concentration of 100 different fatty acid metabolites in the brain tissues of seniors who participated in the Baltimore Longitudinal Study of Aging.
The participants were assessed cognitively in the year prior to their deaths, and their brain tissue was tested for neuropathologies during autopsy.
Legido-Quigley and her colleagues divided the participants into three groups: 14 participants had healthy brains, 15 had a neuropathological buildup of the tau protein or a buildup of amyloid plaque, but no memory problems, and a final group of 14 participants had AD.
Amyloid plaques and tau tangles are abnormal clusters of protein and bundles of fiber, respectively, which are considered to be the main features of AD.
The researchers measured the metabolite levels of the brain regions commonly associated with Alzheimer’s: the middle frontal gyrus and the inferior temporal gyrus. They also examined metabolite levels in a brain area that is not normally affected by Alzheimer’s pathology – the cerebellum.
The study revealed that six unsaturated fatty acids (UFAs) found in the middle frontal and inferior temporal gyri correlated with AD.
The fatty acids shown to correlate with AD in this study were: docosahexaenoic acid, linoleic acid, arachidonic acid, linolenic acid, eicosapentaenoic acid, and oleic acid.
Cristina Legido-Quigley and colleagues explain the significance of the study:
“[This] work suggests that dysregulation of UFA’s metabolism plays a role in driving AD pathology and that these results provide further evidence for the metabolic basis of AD pathogenesis.”
The authors also concede some of the study’s limitations. Due to its observational nature, the research cannot explain causality, so it could not be established whether the UFA dysregulation causes AD or whether it is the other way around.
Additionally, the authors note that larger studies are needed to replicate and confirm the findings. Their study sample was small, as there are not many studies available that examined tissue samples together with cognitive evaluations. Furthermore, the nature of nontargeted metabolomic studies is quite limited, as not all metabolites can be identified at once, so further studies are needed to locate other metabolites.