Diet and Inflammation in Cognitive Ageing and Alzheimer’s Disease

Abstract

Purpose of Review Nutrition is known to modulate the immune system and may alter neuroinflammatory processes implicated in the pathogenesis of Alzheimer's disease (AD) and progression of neurodegeneration. Here, we review the evidence for healthy dietary patterns and age-related cognition and discuss potential neuroinflammatory actions of diet on cognitive function. Recent Findings Anti-inflammatory dietary patterns such as the Mediterranean diet (MD) and dietary approaches to stop hypertension (DASH) may be neuroprotective. Several dietary components consumed in the MD and DASH (omega-3 fatty acids, antioxidants and polyphenols) can inhibit neuroinflammation associated with AD. Anti-inflammatory diets may also attenuate neuroinflammation via indirect immune pathways from the gut microbiome and systemic circulation. Summary Diet may influence cognitive ageing via several inflammatory pathways. However, data from human studies are lacking and the exact mechanisms linking diet to cognitive function remain elusive. Further dietary intervention studies are required to investigate diet-associated neurological change from the earliest through to latest stages of cognitive decline. Furthermore, incorporation of neuroimaging measures in intervention studies would advance current understanding of the mechanistic effects of dietary modification on neuroinflammation in the ageing brain.

Citrulline supplementation improves spatial memory in a murine model for Alzheimer’s disease

“…Accordingly, it has been shown that female mice, rats, and monkeys show stronger antibody [28] and cell-mediated immune responses than males, were estrogens have been suggested to be responsible [29,30]. Inflammation has been strongly implicated in the pathogenesis of AD; production of pro-inflammatory cytokines can perpetuate the cycle of neuroinflammatory processes including amyloidosis, neuronal death, cortical thinning, reduced brain volume, cerebrovascular diseaserelated events, and neurodegeneration [31]. The hypothesis of a direct contribution of the inflammatory response to amyloid plaque progression and, thus, to the neurodegeneration associated with AD [27] could explain the influence of inflammation on cognition.…”

Ficus Erecta Thunb. Leaves Protect Against Cognitive Deficit and Neuronal Damage in a Mouse Model of Amyloid-β-induced Alzheimer’s Disease

“…Neuronal in ammation plays an essential role in facilitating Aβ deposition, neuronal loss, and cognitive de cit [41][42][43]. Many studies suggested that inhibitors of pro-in ammatory cytokines may be a valuable strategy for subverting AD progression in preclinical and clinical trials [44].…”

Pathways of Prevention: A Scoping Review of Dietary and Exercise Interventions for Neurocognition

“…Neuroinflammation is increasingly recognized as having adverse effects on brain [277,278]. Greater levels of circulating neuroinflammatory markers are frequently shown among individuals with ADRD compared to controls, [272,279,280] associate with worsening neurocognition in prospective studies, [281,282] and are upregulated among middle-aged adults with CVD risk factors and obesity [283,284].…”

“…A third potential extension from the present review is the need to carefully account for basal levels of inflammation, which may function as a conceptually central mechanism blocking the effects of indirect mechanistic pathways. Elevated inflammation has been shown to mitigate neurotrophic effects on neurocognition, [421] is common among individuals with CVD risk factors and obesity in particular, [278] has been associated with biomarkers of preclinical ADRD progression, [422] and has been robustly asso-ciated with neurocognitive decline [277]. This could partially explain the lack of neurocognitive improvements in some comprehensive lifestyle trials, such as LOOK-AHEAD [242].…”