Summary: Researchers have identified a pattern of brain change in people with obesity that closely resembles neurodegeneration seen in Alzheimer’s disease. The study suggests that managing excess weight could slow age-related cognitive decline and lower the risk of developing Alzheimer’s.
Source: McGill University
A team at The Neuro (Montreal Neurological Institute-Hospital) of McGill University reports a strong correlation between neurodegeneration patterns in individuals with obesity and those diagnosed with Alzheimer’s disease (AD). Their analysis indicates that excess body weight may contribute to cortical thinning — a marker of neurodegeneration — in brain regions that are also vulnerable in AD. The authors conclude that weight reduction in mid-life could be an actionable strategy to reduce later-life cognitive decline and dementia risk.
Past studies have linked obesity to several Alzheimer’s-related brain changes, including cerebrovascular damage and the buildup of amyloid-β. However, until now, direct comparisons between the anatomical patterns of brain atrophy in obesity and in clinically diagnosed AD had been lacking. This new observational study fills that gap by mapping cortical thickness across a large sample and comparing the spatial patterns of grey matter loss between groups.
Using imaging data from more than 1,300 participants, the researchers created maps of cortical thickness for four groups: people with Alzheimer’s disease, healthy controls, obese but otherwise healthy individuals, and lean individuals. They matched groups by age and sex where appropriate and then compared cortical thickness patterns between AD and controls and between obese and lean participants. Correlation analyses and permutation tests that control for spatial autocorrelation were applied to assess the similarity of atrophy patterns across conditions.
The analysis revealed pronounced overlap in cortical thinning between obesity and AD. Key regions showing similar thinning included the right temporo-parietal cortex and portions of the left prefrontal cortex. Because cortical thinning is commonly interpreted as an indicator of neuronal loss or degeneration, these parallels suggest that obesity may promote the same types of structural brain changes observed in Alzheimer’s.
Obesity is increasingly viewed as a complex multisystem disease that affects respiratory, gastrointestinal, cardiovascular, and other systems. This study, published in the Journal of Alzheimer’s Disease on Jan. 31, 2022, adds evidence of a neurological dimension to that burden, showing that excess weight is associated with structural brain changes that mirror those found in AD and may therefore contribute to dementia risk.
“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: The research was supported by a Foundation Scheme award from the Canadian Institutes of Health Research, computing resources from Calcul Québec and Compute Canada, and 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 credit: Filip Morys
Original Research: Open access. Title: “Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study” by Filip Morys et al., published in the Journal of Alzheimer’s Disease.
Abstract
Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study
Background:
Excess weight during adulthood is already known to increase the likelihood of medical conditions such as diabetes, hypertension, and dyslipidemia. Recent evidence has also linked higher body mass index (BMI) and obesity to brain atrophy and declines in cognitive function. Prior reports have associated obesity with AD-related changes, including cerebrovascular damage and amyloid-β accumulation. However, before this study there had been no direct, large-scale comparison of regional brain atrophy patterns in obesity versus Alzheimer’s disease.
Objective:
The study aimed to compare patterns of cortical thinning and to evaluate the relationship with amyloid-β and tau protein deposition by analyzing imaging data from more than 1,300 individuals representing four groups: AD patients, healthy controls, obese otherwise-healthy participants, and lean participants.
Methods:
Researchers age- and sex-matched each comparison group to the AD patient group and generated cortical thickness maps for both AD-related and obesity-related differences. AD patients were compared with healthy controls, and obese individuals were compared with lean individuals. The resulting maps were analyzed with correlation techniques and permutation-based tests that account for spatial autocorrelation. In addition, obesity-related brain maps were compared with published maps of amyloid-β and tau protein distribution from other studies.
Results:
The cortical thinning maps associated with obesity were highly correlated with those associated with Alzheimer’s disease, indicating strong spatial overlap in affected brain regions. In contrast, the obesity-related maps did not show a significant correlation with published maps of amyloid-β or tau protein deposition. The observed similarity between obesity and AD was not simply due to the presence of obesity among some AD patients.
Conclusion:
This research confirms that the pattern of grey matter atrophy linked to obesity closely resembles that seen in Alzheimer’s disease. These findings reinforce the view that excess weight management could yield important brain-health benefits, potentially slowing cognitive decline with age and lowering the risk of developing dementia and Alzheimer’s disease. Public health efforts that encourage healthy weight in mid-life may therefore contribute to better neurological outcomes in later life.