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Obesity-related neurodegeneration mimics Alzheimer’s disease

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Summary: Researchers have found 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 disease.

Source: McGill university

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A new study by scientists at The Neuro (Montreal Neurological Institute-Hospital) at McGill University finds a correlation between neurodegeneration in obese people and patients with Alzheimer’s disease (AD), suggesting that the loss being overweight could slow cognitive decline in aging and reduce the risk of AD.

Previous research has shown that obesity is linked to Alzheimer’s disease (AD)-related changes, such as cerebrovascular damage and amyloid-β accumulation.

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However, to date, no research has made a direct comparison between patterns of brain atrophy in AD and obesity.

Using a sample of more than 1,300 people, researchers compared patterns of gray matter atrophy in obesity and Alzheimer’s disease.

They compared Alzheimer’s disease patients with healthy controls and obese people with non-obese people, creating maps of gray matter atrophy for each group.

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Scientists found that obesity and Alzheimer’s disease affect cortical gray matter thinning in similar ways. For example, the thinning of the right temporoparietal cortex and the left prefrontal cortex was similar in both groups.

Cortical thinning can be a sign of neurodegeneration. This suggests that obesity can cause the same type of neurodegeneration seen in people with Alzheimer’s disease.

This shows brain scans from the study
A comparison of cortical thickness between the brains of obese patients and those with Alzheimer’s disease. Darker colors indicate similarities in cortical thickness between the two groups. 1 credit

Obesity is increasingly recognized as a multisystem disease affecting the respiratory, gastrointestinal and cardiovascular systems,

among others. Posted in the Alzheimer’s Disease Journal on January 31, 2022, this study also reveals a neurological impact, showing that obesity may play a role in the development of Alzheimer’s disease and dementia.

“Our study reinforces previous literature indicating that obesity is an important factor in AD by showing that cortical thinning could be one of the potential risk mechanisms,” says Filip Morys, PhD researcher at The Neuro and first author of the study.

“Our results underscore the importance of weight reduction in obese and overweight people in mid-life, to reduce the later risk of neurodegeneration and dementia.”

Funding: This study was supported by a Foundation Scheme grant to AD from the Canadian Institutes of Health Research,

computational resources from Calcul Québec and Compute Canada, and a postdoctoral fellowship from the 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
Picture: The image is credited to Filip Morys

Original research: Free access.
“Model of obesity-associated neurodegeneration mimics Alzheimer’s disease in an observational cohort study” by Filip Morys et al. Alzheimer’s Disease Journal


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Model of obesity-associated neurodegeneration mimics Alzheimer’s disease in observational cohort study


Excess weight in adulthood leads to health complications such as diabetes, hypertension or dyslipidemia. Recently, being overweight has also been linked to brain atrophy and cognitive decline. Reports show that obesity is linked to changes related to Alzheimer’s disease (AD), such as cerebrovascular damage or amyloid-β accumulation. However, to date, no research has made a direct comparison between patterns of brain atrophy in AD and obesity.


Here, we compared patterns of brain atrophy and amyloid-β/tau protein accumulation in obesity and AD using a sample of over 1,300 people from four groups: AD patients, healthy controls , otherwise healthy obese people and lean people.

Methods :

We matched all age and sex groups to the AD patient 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 AD and obesity maps using correlation analyzes and permutation-based tests that account for spatial autocorrelation. Similarly, we compared brain maps of obesity with amyloid-β and tau protein maps from other studies.


Obesity maps were strongly correlated with AD maps but not correlated with amyloid-β/tau protein maps. This effect was not explained by the presence of obesity in the AD group.


Our research confirms that obesity-related gray matter atrophy resembles that of AD. Managing excess weight could improve health outcomes, slow age-related cognitive decline, and reduce the risk of Alzheimer’s disease.

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