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Issue title: Healthy Aging and Dementia Research
Guest editors: P. Hemachandra Reddy
Article type: Review Article
Authors: George, Elizabeth Kurudamannilb | Reddy, P. Hemachandraa; b; c; d; e; f; g; *
Affiliations: [a] Internal Medicine Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA | [b] Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, USA | [c] Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, Lubbock, TX, USA | [d] Pharmacology & Neuroscience Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA | [e] Neurology Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA | [f] Speech, Language and Hearing Sciences Department, Texas Tech University Health Sciences Center, Lubbock, TX, USA | [g] Department of Public Health, Graduate School of Biomedical Sciences, Lubbock, TX, USA
Correspondence: [*] Correspondence to: P. Hemachandra Reddy, PhD, Professor of Internal Medicine, Neuroscience & Pharmacology, Neurology and Public Health Departments, Texas Tech University Health Sciences Center, 3601 Fourth Street, Lubbock, TX 79430, USA. E-mail: [email protected]
Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by memory loss and multiple cognitive impairments. Current healthcare costs for over 50 million people afflicted with AD are about $818 million and are projected to be $2 billion by 2050. Unfortunately, there are no drugs currently available that can delay and/or prevent the progression of disease in elderly individuals and in AD patients. Loss of synapses and synaptic damage are largely correlated with cognitive decline in AD patients. Women are at a higher lifetime risk of developing AD encompassing two-thirds of the total AD afflicted population. Only about 1-2% of total AD patients can be explained by genetic mutations in APP, PS1, and PS2 genes. Several risk factors have been identified, such as Apolipoprotein E4 genotype, type 2 diabetes, traumatic brain injury, depression, and hormonal imbalance, are reported to be associated with late-onset AD. Strong evidence reveals that antioxidant enriched diets and regular exercise reduces toxic radicals, enhances mitochondrial function and synaptic activity, and improves cognitive function in elderly populations. Current available data on the use of antioxidants in mouse models of AD and antioxidant(s) supplements in diets of elderly individuals were investigated. The use of antioxidants in randomized clinical trials in AD patients was also critically assessed. Based on our survey of current literature and findings, we cautiously conclude that healthy diets, regular exercise, and improved lifestyle can delay dementia progression and reduce the risk of AD in elderly individuals and reverse subjects with mild cognitive impairment to a non-demented state.
Keywords: Alzheimer’s disease, amyloid-beta, antioxidant enriched diet, healthcare cost, healthy diets, mitochondria, phosphorylated tau, reactive oxygen species, regular exercise
DOI: 10.3233/JAD-190232
Journal: Journal of Alzheimer's Disease, vol. 72, no. s1, pp. S37-S58, 2019
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