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Obesity linked to Alzheimer’s, study finds


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New research has found that brain degeneration in overweight people has similarities to the pattern seen in Alzheimer’s patients. The conclusion is an indication that obesity can cause negative effects on the brain and still be a risk factor for Alzheimer’s.

The article was published on Tuesday (31) in the scientific journal Journal of Alzheimer’s Disease. The group of Canadian researchers had already investigated the relationship between obesity and brain degeneration. In one such study, some organ functions that are affected by dementia, such as memory, were linked to obesity. The point was indicative that being overweight could be associated with Alzheimer’s.

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The new research aimed to further investigate this issue. The scientists used magnetic resonance images from two health banks: the UK biobank, in the United Kingdom, and the Alzheimer’s Neuroimaging Initiative (Adni), with global data on the disease.

These images were used to compare those who already had Alzheimer’s diagnosis with people without the disease, in addition to considering people’s obesity status. In total, 1,300 MRIs were considered and divided into four groups: patients with Alzheimer’s, healthy people (control group), obese individuals without symptoms of dementia, and thin people.

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The focus of the research was the gray matter of the brain, which is associated with functions such as memory and logical reasoning. The objective was to observe whether obesity causes atrophy in this portion of the brain and, if so, to compare it with the pattern observed in Alzheimer’s. In the end, indeed similarities were seen between the two groups.

The obese-only participants, however, still had no symptoms of dementia despite the brain degeneration. Therefore, the loss of brain mass could be an indication that, in the future, these individuals could develop Alzheimer’s – indicating the correlation between the disease and excess weight.

“It is hoped that by treating one, we can prevent the other”, says Cynthia Valério, director of the Brazilian Association for the Study of Obesity and Metabolic Syndrome (Abeso), in reference to the conclusion of the survey. However, she still points out that the point needs to be studied further. “The greatest response we will have in the follow-up of these patients”, she adds.

Valério, who did not sign the study, explains that for research whose purpose is to delimit a cause and effect relationship, the ideal is to adopt a method that follows the participants for years. This was not the case of the recently published study: the analysis was based on a specific period, without following up people with obesity to see if they really had higher rates of Alzheimer’s onset.

The study was also concerned with another aspect related to dementia: the accumulation of beta-amyloid proteins and TAU. The first of these is normally found in the walls of neurons, cells involved in most brain functions. In excess, this protein starts to be deposited in tissues of the organ, something considered as a marker of Alzheimer’s.

Studies already indicate that, years before the onset of symptoms of dementia, it would already be possible to observe an increase in the amount of beta-amyloid.

The concentration of this substance also causes another problem: the retention of TAU, a protein that causes the death of neurons. Because both beta-amyloid and TAU are related to brain degeneration, the researchers chose to also investigate their pattern in cases of obese people. So, it was possible to compare with patients already diagnosed with Alzheimer’s and conclude if there is any correlation.

In the case of these proteins, the researchers found no association between obesity and their increase. For Valerio, this demonstrates the complexity of ways that may be involved in the onset of Alzheimer’s.

“The atrophy seen on the brain map was from other regions and markers other than [as proteínas beta-amiloide e TAU que são] more specific”, he concludes.

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