Fat Can Secretly Contribute To Alzheimer’s Disease: Study

While obesity has long been recognised as a contributor to various illnesses, the exact connection between excess weight and Alzheimer’s disease has, until recently, remained unclear. 

A pioneering study from Houston Methodist has discovered that extracellular vesicles originating from fat tissue act as tiny messengers, prompting the accumulation of amyloid-β plaques in individuals with obesity. These plaques are an important characteristic of Alzheimer’s disease.

The study titled, “Decoding Adipose-Brain Crosstalk: Distinct Lipid Cargo in Human Adipose-Derived Extracellular Vesicles Modulates Amyloid Aggregation in Alzheimer's Disease”, was published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association on Oct. 2.

The study examines the connection between obesity, which affects roughly 40% of the US population and Alzheimer’s disease that impacts over 70 lakh Americans.

The research was spearheaded by Stephen Wong, who holds the John S. Dunn Presidential Distinguished Chair in Biomedical Engineering at Houston Methodist.

"As recent studies have underscored, obesity is now recognised as the top modifiable risk factor for dementia in the United States," said Wong, as per a report in ScienceDaily.

The research revealed that the lipid composition of these cellular messengers varies significantly between individuals with obesity and those who are lean. Moreover, the specific lipids present and their quantities in each group influence how rapidly amyloid-β proteins aggregate in laboratory experiments. It sheds light on potential mechanisms linking obesity to Alzheimer’s disease.

Using mouse models and samples of body fat from patients, the team studied vesicles, which are minute, membrane-enclosed particles that circulate throughout the body and facilitate communication between cells. Remarkably, these tiny messengers can also pass through the blood-brain barrier to reach the brain.

Interrupting the communication of these tiny cellular messengers, which contribute to plaque formation, could prove beneficial in lowering the risk of Alzheimer’s disease among individuals with obesity.

The researchers emphasised that future studies should prioritise exploring how drug treatments might halt or slow the accumulation of toxic proteins linked to Alzheimer’s, such as amyloid-β, in individuals at risk.