The Impact of Medium Chain and Polyunsaturated ω-3-Fatty Acids on Amyloid-β Deposition, Oxidative Stress and Metabolic Dysfunction Associated with Alzheimer's Disease.

Janine Mett

doi:10.3390/antiox10121991

Abstract

Alzheimer’s disease (AD), the most common cause of dementia in the elderly population, is closely linked to a dysregulated cerebral lipid homeostasis and particular changes in brain fatty acid (FA) composition. The abnormal extracellular accumulation and deposition of the peptide amyloid-β (Aβ) is considered as an early toxic event in AD pathogenesis, which initiates a series of events leading to neuronal dysfunction and death. These include the induction of neuroinflammation and oxidative stress, the disruption of calcium homeostasis and membrane integrity, an impairment of cerebral energy metabolism, as well as synaptic and mitochondrial dysfunction. Dietary medium chain fatty acids (MCFAs) and polyunsaturated ω-3-fatty acids (ω-3-PUFAs) seem to be valuable for disease modification. Both classes of FAs have neuronal health-promoting and cognition-enhancing properties and might be of benefit for patients suffering from mild cognitive impairment (MCI) and AD. This review summarizes the current knowledge about the molecular mechanisms by which MCFAs and ω-3-PUFAs reduce the cerebral Aβ deposition, improve brain energy metabolism, and lessen oxidative stress levels.

Highlights

NT—Natural Science and Technology, Saarland University, D-66123 Saarbrücken, Germany; Citation: Mett, J
medium chain fatty acids (MCFAs)-derived ketone bodies might serve as an alternative fuel in the brain of Alzheimer’s disease (AD) patients compensating for the lack of cerebral glucose utilization [1]
A body of evidence supports the fact that the dietary supplementation of ω-3-Polyunsaturated fatty acids (PUFAs) and MCFAs could be valuable for disease modification

Summary

Fatty Acids

50% of the human brain’s dry weight consists of lipids, making it the second most lipid-rich organ in the body after adipose tissue. The diversity of lipids is mainly based on the variation of fatty acids (FAs) which can differ in the length and saturation degree of their hydrocarbon chain. This determines their physical properties such as their melting point [1]. Shorter-chained and unsaturated FAs have the opposite effect Such alterations in the biophysical properties of cellular membranes can affect the trafficking of cellular constituents, membrane protein function, and signal propagation [12,13]. In the following chapters of this article, I will summarize the current knowledge about the impact of these special FAs on the molecular mechanisms that are associated with AD focusing on amyloid-β (Aβ) deposition, oxidative stress, and neuronal energy metabolism dysfunction

Alzheimer’s Disease

The Impact of ω-3-PUFAs and MCFAs on Aβ Deposition

The Impact of ω-3-PUFAs and MCFAs on Oxidative Stress

The Impact of ω-3-PUFAs and MCFAs on Neuronal Energy Metabolism

Findings

Conclusions