Fatting the brain: a brief of recent research

Abstract

Fatty acids are of paramount importance to all cells, since they provide energy, function as signaling molecules, and sustain structural integrity of cellular membranes. In the nervous system, where fatty acids are found in huge amounts, they participate in its development and maintenance throughout life. Growing evidence strongly indicates that fatty acids in their own right are also implicated in pathological conditions, including neurodegenerative diseases, mental disorders, stroke, and trauma. In this review, we focus on recent studies that demonstrate the relationships between fatty acids and function and dysfunction of the nervous system. Fatty acids stimulate gene expression and neuronal activity, boost synaptogenesis and neurogenesis, and prevent neuroinflammation and apoptosis. By doing so, they promote brain development, ameliorate cognitive functions, serve as anti-depressants and anti-convulsants, bestow protection against traumatic insults, and enhance repairing processes. On the other hand, unbalance between different fatty acid families or excess of some of them generate deleterious side effects, which limit the translatability of successful results in experimental settings into effective therapeutic strategies for humans. Despite these constraints, there exists realistic evidence to consider that nutritional therapies based on fatty acids can be of benefit to several currently incurable nervous system diseases.

The Relationship between Fatty Acids and Different Depression-Related Brain Regions, and Their Potential Role as Biomarkers of Response to Antidepressants

“…Briefly, fatty acids are classified based on the number of double bonds (i.e., the degree of saturation/unsaturation) in the carbon chain into saturated (SFA; no double bonds), monounsaturated (MUFA; one double bond), or polyunsaturated (PUFA; two or more double bounds) [13]. PUFAs are further distinguished based on the position of the first double bond from the methyl terminal end into n -3 or n -6 PUFAs.…”

“…This is notable given that brain insulin resistance promotes depression-like behavior in rodents [45]. Furthermore, low MUFA levels have been associated with the development of Alzheimer’s disease, as suggested by findings that MUFA levels, especially oleic acid, are reduced in the brain of Alzheimer’s patients [13]. Importantly, depression is commonly observed in Alzheimer’s patients [46].…”

Aberrant Lipid Metabolism in the Forebrain Niche Suppresses Adult Neural Stem Cell Proliferation in an Animal Model of Alzheimer’s Disease

“…Indeed, lipid accumulations were one of the five original AD-associated tissue pathologies reported by Alois Alzheimer (Alzheimer, 1907). More recently, links have strengthened between aberrant lipid metabolism and neurodegeneration in AD (Astarita et al, 2011;Fraser et al, 2010;Hussain et al, 2013;Podtelezhnikov et al, 2011;Tanzi, 2012), while epidemiological studies have demonstrated that AD risk factors include peripheral metabolic conditions such as insulin resistance, obesity, and dyslipidemia (Pasinetti and Eberstein, 2008). However, deeper mechanistic insights into the role of abnormal lipid metabolism in AD have been hindered by the technical complexity involved with localizing, identifying, and determining the biological functions of individual lipid species in the brain.…”

Factors affecting the ability of baclofen to reduce fat intake in rats

“…These results demonstrate that the presence of an alternative food option does not influence the ability of baclofen to reduce shortening intake. Why consumption of shortening and lard would be differentially affected by baclofen under the experimental conditions reported here is not clear, but may be due to the differential fatty acid composition of the two fats (Hussain et al, 2013). Future studies will need to be conducted in which dietary fatty acid composition is systematically manipulated and effects on baclofen pharmacokinetics and pharmacodynamics are assessed.…”