Abstract
Many theories have been proposed to explain why candidate disease-modifying drugs (DMTs) for Alzheimer's disease (AD) failed. Late initiation of treatments during AD development, inappropriate drug dosages, incorrect selection of main therapeutic targets, and primarily inadequate understanding of the complex pathophysiology of AD are the most prominent ones. Reduced expression of Brain Derived Neurotrophic Factor (BDNF) is essential in the pathogenesis of Alzheimer's disease. BDNF plays important functions in cell survival and differentiation, neuronal outgrowth and plasticity. It can be a novel target for the treatment of the disease. In Alzheimer's disease, the hippocampus, parietal, entorhinal, and frontal cortex all have the most extreme BDNF deficits. Lower levels of BDNF can be linked to neuronal death, masking any gene-related effects. High BDNF levels have been attributed to a lower risk of dementia and Alzheimer's. Improvements in BDNF levels imparted by exercise, plant based drugs, trkB receptor agonist and BDNF enhancer drug have been proved to enhance cognitive performance. Plant-based products and nutraceuticals can boost BDNF levels. Polyphenols are essential plant compounds with a wide range of therapeutic potentials. Flavonoids like calycosin, genistein, isorhamnetin, and luteolin have been shown to affect the level of BDNF. Curcumin, a compound derived from spice turmeric (curcuma longa), has a variety of biological functions in the brain, including antidepressant properties which also increase BDNF level in the hippocampus. Riluzole is used to treat amyotrophic lateral sclerosis (ALS). In a depression model with chronic corticosteroid intake, riluzole also restores hippocampal BDNF levels. Evidence indicates that BDNF deficiency plays a role in the pathogenesis of Alzheimer's disease. Drugs used to treat Alzheimer's disease have the unintended property of modulating BDNF levels in brain regions specifically involved in the disease's pathophysiology. The discovery of molecules that precisely control BDNF in particular cellular phenotypes could increase the effectiveness of therapy against AD.
Highlights
Living activities are fundamental skills required to independently care for oneself and are categorized in basic and instrumental activities of daily living
These findings indicate that vitamin E supplementation could be a developing therapeutic choice for diseases characterised by oxidative damage, such as Alzheimer's disease, by enhancing the brain-derived neurotrophic factor (BDNF) and cAMP response element binding protein (CREB) pathways [135]
Evidence indicates that BDNF deficiency plays a role in the pathogenesis of Alzheimer's disease
Summary
Living activities are fundamental skills required to independently care for oneself and are categorized in basic and instrumental activities of daily living. Brain-derived neurotrophic factor (BDNF) is sometimes denoted as miracle grow for the brain” because several studies have reported that BDNF nourishes neurons like that of the fertilizer nourishes a plant [9,10]. It is well-known that BDNF protects brain cells and stimulates growth of their dendrites and axons. BDNF acts on certain neurons of the central nervous system and the peripheral nervous system, helping to support survival of existing neurons, and encouraging growth and differentiation of new neurons and synapses In the brain it is active in the hippocampus, cortex and basal forebrain—areas vital to learning, memory and higher thinking. Studies suggest that neurotrophic factors have a protective role against amyloid beta toxicity [7,8,9,10,11,12,13]
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