Brain-Derived Neurotrophic Factor: A Connecting Link Between Nutrition, Lifestyle, and Alzheimer’s Disease

Abstract

Brain-derived neurotrophic factor (BDNF) involving tropomyosin kinase B and low affinity p75 neurotropin receptors is the most abundant and researched neurotropins in mammal’s brain. It is one of the potential targets for therapeutics in Alzheimer’s disease (AD) owing to its key role in synaptic plasticity. Low levels of BDNF are implicated in the pathophysiology of neurological diseases including AD. However, a healthy lifestyle, exercise, and dietary modifications are shown to positively influence insulin regulation in the brain, reduce inflammation, and up-regulate the levels of BDNF, and are thus expected to have roles in AD. In this review, the relationship between BDNF, mental health, and AD is discussed. Insights into the interrelationships between nutrition, lifestyle, and environment with BDNF and possible roles in AD are also provided in the review. The review sheds light on the possible new therapeutic targets in neurodegenerative diseases.

Effectiveness of non-pharmacological therapies on cognitive function in patients with dementia—A network meta-analysis of randomized controlled trials

“…A large number of RCTs had reported the positive effects of exercise on cognitive function in patients with dementia ( Henskens et al, 2018 ; Lamb et al, 2018 ; de Oliveira Silva et al, 2019 ). Exercise therapy improved cognitive performance mechanisms, such as increasing growth factors ( Ruiz-González et al, 2021 ; Xue et al, 2022 ), modulating inflammatory cytokines ( Hashiguchi et al, 2020 ; de Farias et al, 2021 ), alleviating oxidative stress ( Hu et al, 2022 ), increasing cerebral blood flow ( Lu et al, 2019 ; Tomoto et al, 2021 ), decreasing antibody concentrations ( Giménez-Llort et al, 2013 ), and inhibiting tau phosphorylation from slowing the progression of dementia ( Wang et al, 2021 ; Xu et al, 2022 ). However, these potential mechanisms have been proved to exist only in animal models, and some studies examining these mechanisms have not yet to prove their applicability to humans.…”

The Role of Mitochondrial Dysfunction in Alzheimer’s: Molecular Defects and Mitophagy-Enhancing Approaches

“…In AD mouse models, PE exhibited helpful properties on synaptic plasticity modifications, reestablished neuroprotective feature altitudes, amended cognitive shortages, and decreased Aβ assembly [120]. Frequent trials recommended that PE be represented via the SIRT1/PINK1/Parkin cascade way [121,122]. In addition, PE for APP/PS1 mice augmented mitophagy, improved knowledge and memory capabilities, synaptic action, Aβ burden, and mitochondrial functionality, and reduced OS markers [123].…”

Docosahexaenoic Acid (DHA), Vitamin D3, and Probiotics Supplementation Improve Memory, Glial Reactivity, and Oxidative Stress Biomarkers in an Aluminum-Induced Cognitive Impairment Rat Model

“…Studies have verified that the adequate consumption of DHA has protective properties, showcasing its ability to limit synaptic loss, cognition defects, and even suppress neural damage promoted by amyloid β and hyperphosphorylated tau accumulation in Alzheimer’s disease models. − Vitamin D has shown neuroprotective potential in several studies through its involvement in antioxidant pathways, neurotrophin production, neuronal calcium and glutamate regulation, immunomodulation, and amyloid β clearance. − Probiotics, influencing the gut-brain axis, are emerging as biotherapies for neurodegenerative diseases, positively impacting neurotrophic factors and reducing oxidative stress, influencing neuronal plasticity. ,− …”