Ways To Prevent Alzheimer's Disease – Dementia is a growing public health problem, affecting an estimated 57 million adults worldwide. Alzheimer’s disease (AD) accounts for 60-80% of cases. Clinical trials testing potential drugs and neuroprotective agents have been inconclusive, and approved drugs provide only symptomatic benefits. Emerging epidemiological and clinical studies suggest that lifestyle changes, including diet and physical activity, offer an alternative therapeutic approach to slowing and preventing cognitive decline and dementia. Age is the most common risk factor for dementia and is associated with a decline in cellular bioenergetics and metabolic processes. Therefore, a nutrient-dense diet is essential for optimal brain health. Furthermore, type 2 diabetes (T2D) is a risk factor for AD, and diets that reduce the risk of T2D may provide neuroprotection. Predominant foods in the Mediterranean, MIND, and DASH diets, including fruits, leafy greens, fish, nuts, and olive oil, may prevent or slow cognitive decline. The mechanisms by which these nutrients promote brain health are not yet fully understood. Other dietary approaches and eating patterns, including ketogenic and intermittent fasting, are also beneficial for brain health. This review summarizes the pathophysiology, associated risk factors, and potential neuroprotective pathways activated by various diets and eating patterns that show promise in promoting brain health and preventing dementia.
With age being the main risk factor for dementia and life expectancy increasing, the global burden of this devastating condition is expected to increase exponentially. According to the 2019 Global Burden of Disease (GBD) study, disability-adjusted life years (DALYs) of Alzheimer’s disease (AD) and other dementias account for 4.3% of total DALYs (2.02-9.7%) worldwide and 5 make up .3%. DALYs (2.66-10.86%) in the United States for persons aged 70 and older (Institute for Health Metrics and Evaluation GBD2019).
Ways To Prevent Alzheimer's Disease
The number of people with dementia is projected to increase from 57.4 (95% CI 50.4-65.1) million cases worldwide to 152.8 (130.8-175.9) million cases by 2019. 2050 to increase (1). AD is the most common form of dementia and accounts for at least two-thirds of dementia cases in patients aged 65 years and older (2). Therefore, AD and other forms of dementia are expected to represent a significant health burden worldwide.
Down Syndrome And Alzheimer’s Disease: Common Molecular Traits Beyond The Amyloid Precursor Protein
According to the World Health Organization (WHO), AD is a progressive disease divided into three clinical stages. The first stage is mild cognitive impairment (MCI), an intermediate stage between normal cognitive functioning and overt AD dementia. MCI affects the memory of individuals with or without affecting their daily life (3). Examples of MCI include losing things and forgetting to show up for meetings. MCI can persist throughout life or progress to mild, moderate, and advanced forms of AD. In other words, MCI can be considered a precursor to AD. Advanced AD symptoms include forgetfulness of long-term memories and loved ones and difficulty performing daily activities such as eating, toileting, and dressing.
There is currently no cure for AD. Several drugs have been studied as neuroprotective agents for AD. For example, cholinesterase inhibitors, which increase the availability of acetylcholine, may slow the progression of cognitive decline; however, there is no strong evidence that these treatments are neuroprotective or slow the course of the disease (4, 5). Another drug studied, memantine, is a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) glutamate receptors, which play a role in learning and memory (6, 7). Excessive NMDA stimulation can lead to neurotoxicity (8). Memantine can block pathological stimulation of NMDA receptors. A review of the literature suggests that the effects of memantine may be subtle and often not clinically significant (9). Another line of drugs, monoamine oxidase (MAO) inhibitors, can reduce the production of neurotoxic compounds (10). Recently, aducanumab and lecanemab, antibodies directed against amyloid beta (Aβ), the main component of amyloid plaques, have received much attention based on promising results from a meta-analysis of the results of several clinical trials (11). However, in a recent study with lecanemab, clinical benefit was modest and associated with significant adverse events (12, 13). Some cholesterol transporters have also been implicated in amyloid transport in the brain; therefore, these pathways are also considered potential therapeutic targets (10). Interestingly, as of January 2022, there were 143 potential therapeutic agents in the AD drug development pipeline (14). Unfortunately, most clinical trials have proven futile, and some drugs only relieve symptoms. Due to the lack of treatments that can delay the onset and slow the progression of AD, it is important to investigate lifestyle changes that can reduce the risk and/or modify the course of the disease.
AD is a highly complex disease involving multiple genetic and environmental factors, some of which are modifiable. Genetically, there are monogenic and polygenic forms of the disease, the latter accounting for more than 95% of cases (15). In other words, most cases of AD are not explained by a single genetic cause, but are influenced by multiple genes in combination with lifestyle and environmental factors. About one-third of AD cases may be related to low education, smoking, alcohol consumption, depression, diabetes, hypertension, obesity, and physical inactivity (16). Recent advances in network medicine have revealed common molecular and pathophysiological mechanisms shared between AD and other comorbidities (17). A hypothesis for the development of AD has been proposed based on genomics (GWAS, genome/exome sequencing, targeted gene sequencing and functional genomics), transcriptomics (microarray and RNA-seq), radiomics (brain imaging), pharmacogenomics (pharmaceuticals). Drug Targeting Network and Gene Signatures) and interactome (protein-protein interactome) that define six endophenotypes, including amyloidosis, tauopathy, neuroinflammation, mitochondrial dysfunction, vascular dysfunction, and lysosomal dysfunction (18). The risk and rate of progression of most and perhaps all of these AD endophenotypes should respond positively to healthy habits related to lifestyle medicine, including good nutrition, physical activity, adequate quality sleep, social engagement, and avoidance of exposure to air. pollution and secondhand smoke, smoking cessation and reducing alcohol consumption (19, 20). A summary of the six pillars of lifestyle medicine is shown in Figure 1.
Figure 1. Components of lifestyle medicine. Lifestyle medicine focuses on six pillars of a healthy lifestyle: nutrition, exercise, stress management, social support, sleep, and avoiding risky behaviors such as smoking. Following the six pillars is expected to reduce the risk of Alzheimer’s disease.
Alzheimer’s Disease Drug Development Pipeline: 2020
AD is associated with a wide range of comorbidities (17). T2D and cardiovascular disease are among the most common diseases with the most adverse effects in patients with AD. T2D is the most prevalent metabolic disorder, affecting approximately 462 million people worldwide (21). AD and T2D share common risk factors, including but not limited to obesity, physical inactivity, depression, family history of diabetes, heart disease, hypertension, or stroke.
In both men and women, those with T2D have an approximately 60% greater risk of developing dementia than those without T2D (22). For this reason, AD is often called type 3 diabetes. Insulin resistance negatively affects cognition (23). Too much insulin leads to the availability of glucose and fat, which can increase reactive oxygen species, which can negatively affect brain health (24). Therefore, health care providers should assess the risk of MCI and AD in patients with T2D, cardiovascular disease, kidney disease, and other complications. For example, the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) provide valuable information about the patient’s cognitive state that the doctor can use to guide him in making specific lifestyle changes that the patient can implement. An important and modifiable risk factor for AD is a healthy diet. Evidence from epidemiological studies suggests that certain nutrients that reduce the risk of T2D may have a protective effect against AD (25). For example, following a Mediterranean diet that includes staple foods such as fish, olive oil, fruits, and green leafy vegetables may reduce the risk of AD and cognitive decline (26).
Although the molecular mechanisms linking T2D and MCI to AD are not fully understood, several studies have revealed common pathways and features between the two diseases. For example, amyloid and tau proteins are common molecular pathological features in AD and T2D (27). Furthermore, transcription factors that turn genes on or off regulate gene expression similarly in AD and T2D ( 28 ). In particular, inflammation, insulin and glucose metabolism, as well as phosphatidylinositol 3-kinase and protein kinase B/Akt (PI3K-AKT) play a central role in the development of T2D and AD (28). Therefore, targets shared between both diseases may lead to new therapeutic treatments for AD.
Brain degeneration is a pathophysiological change shared between MCI, AD, and T2D (29). In particular, medial temporal atrophy is a common finding in MCI and AD (30). Neuroimaging studies have reported that diabetes is also associated with lower total brain volume and reduced executive function in individuals without cerebrovascular disease or dementia (31, 32). Furthermore, chronic hypovolemia, possibly due to dehydration, is present in diabetes, hypertension, and AD (33). In addition, total body water decreases with age (34). Therefore, drinking more water restores the brain (35). Clinical studies are needed to determine whether drinking enough fluids to stay hydrated can reduce or prevent stroke.
Trial Of The Mind Diet For Prevention Of Cognitive Decline In Older Persons
Growing evidence also suggests a link between AD and atherosclerosis, the buildup of fat in the arteries that can result from chronic poor food choices. One
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