Abstract
Alzheimer’s disease (AD) is a type of incurable neurodegenerative disease that is characterized by the accumulation of amyloid-β (Aβ; plaques) and tau hyperphosphorylation as neurofibrillary tangles (NFTs) in the brain followed by neuronal death, cognitive decline, and memory loss. The high prevalence of AD in the developed world has become a major public health challenge associated with social and economic burdens on individuals and society. Due to there being limited options for early diagnosis and determining the exact pathophysiology of AD, finding effective therapeutic strategies has become a great challenge. Several possible risk factors associated with AD pathology have been identified; however, their roles are still inconclusive. Recent clinical trials of the drugs targeting Aβ and tau have failed to find a cure for the AD pathology. Therefore, effective preventive strategies should be followed to reduce the exponential increase in the prevalence of cognitive decline and dementia, especially AD. Although the search for new therapeutic targets is a great challenge for the scientific community, the roles of lifestyle interventions and nutraceuticals in the prevention of many metabolic and neurodegenerative diseases are highly appreciated in the literature. In this article, we summarize the molecular mechanisms involved in AD pathology and the possible ameliorative action of lifestyle and nutritional interventions including diet, exercise, Calorie restriction (CR), and various bioactive compounds on cognitive decline and dementia. This article will provide insights into the role of non-pharmacologic interventions in the modulation of AD pathology, which may offer the benefit of improving quality of life by reducing cognitive decline and incident AD.
Highlights
Due to improved healthcare infrastructures and early diagnosis of diseases, human life expectancy is increasing globally (Oeppen and Vaupel, 2002)
Alzheimer’s disease (AD), the most dominant form of dementia, accounting for 60–80% of dementia cases, is a multifactorial neurodegenerative disease characterized by the accumulation of amyloid-β (Aβ; plaques) outside neurons and the hyperphosphorylation of tau protein and neurofibrillary tangles (NFTs) inside the neurons in the brain, which lead to cognitive deficit, memory loss, and neuron death
We focus on the molecular mechanisms involved in AD and the lifestyle and nutritional interventions, such as physical exercise, a Mediterranean diet (MD), nutraceuticals, and bioactive compounds, as preventive strategies for the development of AD in the elderly population
Summary
Due to improved healthcare infrastructures and early diagnosis of diseases, human life expectancy is increasing globally (Oeppen and Vaupel, 2002). We focus on the molecular mechanisms involved in AD and the lifestyle and nutritional interventions, such as physical exercise, a Mediterranean diet (MD), nutraceuticals, and bioactive compounds, as preventive strategies for the development of AD in the elderly population These interventions for the prevention or delay of the onset of dementia could have significant effects on individuals, society, and healthcare providers. Every 10th American aged above 65 years is suffering from AD This increase in the incidence and prevalence of AD in the elderly population has become a major public health challenge associated with an economic burden on individuals, society, caregivers, and federal governments (Hurd et al, 2013). Reducing the potentially modifiable risk determinants, including educational status, cigarette smoking, sedentary lifestyle, depression, hypertension, diabetes, dyslipidemia, and obesity, may help in the prevention of about 500,000 cases of dementia in the United States (GBD 2015 Neurological Disorders Collaborator Group, 2017)
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