Research from Qingdao University, China, reported how disrupted fat metabolism might contribute to the development and progression of Alzheimer’s disease (AD).
Research in recent years has yielded a growing body of evidence linking AD to metabolic syndrome (MetS), a cluster of simultaneously-occurring conditions which includes diabetes, obesity, high blood pressure and abnormal blood fat levels or dyslipidaemia.
The brain is largely composed of lipids, which are crucial for maintaining the structure and function of neurons, By knowing the connections between MetS and AD, and the specific mechanisms by which dyslipidaemia contributes to AD, it will be possible to identify new treatment targets and potentially develop therapeutic strategies in the future.
The relationship between obesity and AD presents a complex picture, with timing apparently playing a crucial role. Research indicates that being overweight in the middle years, rather than in later life, may be more strongly linked to the development of different forms of dementia and cognitive decline. Brain scans of obese individuals have revealed changes similar to those seen in AD, including reductions in gray matter volume.
Perhaps most intriguingly, the review highlights how dyslipidaemia may play a central role in connecting these various conditions to AD. Various past analyses have found links between dysregulation in the metabolism of cholesterol and fatty acids with harmful brain or neuronal conditions. These include neuronal inflammation, Aβ protein buildup, blood-brain barrier breakdown, and oxidative stress, which were all analysed in detail from a molecular biology perspective in the article.
Importantly, this literature review points to the fact that maintaining healthy blood fat levels may be more important for brain health than previously thought. Promising preventive or therapeutic strategies that are currently under study even include cholesterol-lowering medications and dietary approaches, such as Mediterranean and ketogenic diets and omega-3 fatty acid supplementation.