Summary: Researchers discovered a correlation between obesity-related neurodegeneration and Alzheimer’s disease pathology. Losing weight, they say, can slow age-related cognitive decline and reduce the risk of developing Alzheimer’s.
Source: McGill University
A new study led by scientists at The Neuro (Montreal Neurological Institute-Hospital) of McGill University finds a correlation between neurodegeneration in obese people and Alzheimer’s disease (AD) patients, suggesting that losing excess weight could slow cognitive decline in aging and lower risk for AD.
Previous research has shown that obesity is linked with Alzheimer’s disease (AD)-related changes, such as cerebrovascular damage and amyloid-β accumulation. However, to date no research has made a direct comparison between brain atrophy patterns in AD and obesity.
Using a sample of over 1,300 individuals, the researchers compared patterns of grey matter atrophy in obesity and AD. They compared the AD patients with healthy controls, and obese with non-obese individuals, creating maps of grey matter atrophy for each group.
The scientists found that obesity and AD affected grey matter cortical thinning in similar ways. For example, thinning in the right temporo-parietal cortex and left prefrontal cortex were similar in both groups. Cortical thinning may be a sign of neurodegeneration. This suggests that obesity may cause the same type of neurodegeneration as found in people with AD.
Obesity is increasingly recognized as a multisystem disease affecting respiratory, gastrointestinal, and cardiovascular systems, among others. Published in the Journal of Alzheimer’s Disease on Jan. 31, 2022, this study helps reveal a neurological impact as well, showing obesity may play a role in the development of Alzheimer’s and dementia.
“Our study strengthens previous literature pointing to obesity as a significant factor in AD by showing that cortical thinning might be one of the potential risk mechanisms,” says Filip Morys, a PhD researcher at The Neuro and the study’s first author. “Our results highlight the importance of decreasing weight in obese and overweight individuals in mid-life, to decrease the subsequent risk of neurodegeneration and dementia.”
Funding: This study was funded with a Foundation Scheme award to AD from the Canadian Institutes of Health Research, computing resources from Calcul Quebec and Compute Canada, and by a postdoctoral fellowship from Fonds de Recherche du Québec – Santé.
About this obesity and Alzheimer’s disease research news
Author: Shawn Hayward
Source: McGill University
Contact: Shawn Hayward – McGill University
Image: The image is credited to Filip Morys
Original Research: Open access.
“Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study” by Filip Morys et al. Journal of Alzheimer’s Disease
Abstract
See also
Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study
Background:
Excess weight in adulthood leads to health complications such as diabetes, hypertension, or dyslipidemia. Recently, excess weight has also been related to brain atrophy and cognitive decline. Reports show that obesity is linked with Alzheimer’s disease (AD)-related changes, such as cerebrovascular damage or amyloid-β accumulation. However, to date no research has conducted a direct comparison between brain atrophy patterns in AD and obesity.
Objective:
Here, we compared patterns of brain atrophy and amyloid-β/tau protein accumulation in obesity and AD using a sample of over 1,300 individuals from four groups: AD patients, healthy controls, obese otherwise healthy individuals, and lean individuals.
Methods:
We age- and sex-matched all groups to the AD-patients group and created cortical thickness maps of AD and obesity. This was done by comparing AD patients with healthy controls, and obese individuals with lean individuals. We then compared the AD and obesity maps using correlation analyses and permutation-based tests that account for spatial autocorrelation. Similarly, we compared obesity brain maps with amyloid-β and tau protein maps from other studies.
Results:
Obesity maps were highly correlated with AD maps but were not correlated with amyloid-β/tau protein maps. This effect was not accounted for by the presence of obesity in the AD group.
Conclusion:
Our research confirms that obesity-related grey matter atrophy resembles that of AD. Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.
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