During the past century, treatments for the diseases of youth and middle age have helped raise life expectancy significantly. However, cognitive decline has emerged as one of the greatest health threats of old age, with nearly 50% of adults over the age of 85 afflicted with Alzheimer's disease. Developing therapeutic interventions for such conditions demands a greater understanding of the processes underlying normal and pathological brain ageing. Recent advances in the biology of ageing in model organisms, together with molecular and systems-level studies of the brain, are beginning to shed light on these mechanisms and their potential roles in cognitive decline.

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Neural mechanisms of ageing and cognitive decline

It has long been suspected that the relative abundance of specific nutrients can affect cognitive processes and emotions. Newly described influences of dietary factors on neuronal function and synaptic plasticity have revealed some of the vital mechanisms that are responsible for the action of diet on brain health and mental function. Several gut hormones that can enter the brain, or that are produced in the brain itself, influence cognitive ability. In addition, well-established regulators of synaptic plasticity, such as brain-derived neurotrophic factor, can function as metabolic modulators, responding to peripheral signals such as food intake. Understanding the molecular basis of the effects of food on cognition will help us to determine how best to manipulate diet in order to increase the resistance of neurons to insults and promote mental fitness.

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Brain foods: the effects of nutrients on brain function

https://www.healthpromoting.com/sites/default/files/FastingMolecularMechanisms.pdf

Fasting: Molecular Mechanisms and Clinical Applications

https://www.cell.com/trends/neurosciences/pdf/S0166-2236(08)00163-X.pdf

Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease.

IW Hamley Chemical reviews, 2012 ACS Publications ... the γ-secretase complex and its cell surface localization, in the absence of an effect on Notch ... in the development of effective γ-secretase inhibitors is to avoid side-effects caused by ... EP2 receptor.(79) Prostaglandin E 2 is produced during inflammation due to activity by cytosolic ... Cited by 143 Related articles All 4 versions Cite Save

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Veerendra Kumar Madala Halagappa

Papers

Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer's disease.

Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice.