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Alzheimer’s disease: the role of extrinsic factors in its development, an investigation of the environmental enigma
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This review examines how environmental contaminants, including microplastics, may contribute to Alzheimer's disease risk. Along with air pollutants, toxic metals, and pesticides, plastics and microplastics are identified as potential risk factors that may promote brain inflammation and neurodegeneration. The review explores the molecular mechanisms behind these effects and suggests strategies to reduce the brain health impacts of environmental contaminants.
In the realm of Alzheimer's disease, the most prevalent form of dementia, the impact of environmental factors has ignited intense curiosity due to its substantial burden on global health. Recent investigations have unveiled these environmental factors as key contributors, shedding new light on their profound influence. Notably, emerging evidence highlights the detrimental role of various environmental contaminants in the incidence and progression of Alzheimer's disease. These contaminants encompass a broad spectrum, including air pollutants laden with ozone, neurotoxic metals like lead, aluminum, manganese, and cadmium, pesticides with their insidious effects, and the ubiquitous presence of plastics and microplastics. By meticulously delving into the intricate web connecting environmental pollutants and this devastating neurological disorder, this comprehensive chapter takes a deep dive into their involvement as significant risk factors for Alzheimer's disease. Furthermore, it explores the underlying molecular mechanisms through which these contaminants exert their influence, aiming to unravel the complex interactions that drive the pathogenesis of the disease. Additionally, this chapter proposes potential strategies to mitigate the detrimental effects of these environmental contaminants on brain health, with the ultimate goal of restoring and preserving typical cognitive function. Through this comprehensive exploration, we aim to enhance our understanding of the multifaceted relationship between neurotoxins and Alzheimer's disease, providing a solid foundation for developing innovative in-vivo models and advancing our knowledge of the intricate pathological processes underlying this debilitating condition.
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This review examined the role of emerging environmental contaminants, including microplastics, in the development and progression of Alzheimer's disease. The authors discussed mechanisms including oxidative stress, neuroinflammation, and blood-brain barrier disruption as potential pathways linking environmental exposures to AD pathogenesis.
[Environmental pollutants and Alzheimer's disease].
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This review examines how common environmental pollutants — including heavy metals, pesticides, and microplastics — contribute to Alzheimer's disease risk by damaging neurons, triggering inflammation, and promoting the hallmark protein buildups (amyloid-beta and tau) seen in the disease. Microplastics are identified as an emerging neurotoxic pollutant alongside more established chemicals. The evidence adds to growing concern that everyday environmental exposures, not just genetics, play a meaningful role in driving dementia.
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This review examines emerging evidence that chronic microplastic exposure may be a previously overlooked risk factor for dementia. Microplastics can cross the blood-brain barrier and may promote brain damage through oxidative stress, inflammation, and by accelerating the buildup of amyloid plaques linked to Alzheimer's disease, with studies finding higher microplastic levels in the brains of dementia patients compared to controls.
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This review summarizes existing research on how pollutants, including air pollution, heavy metals, pesticides, and micro- and nanoplastics, may enter the brain and contribute to processes linked to Alzheimer's disease, such as protein buildup and inflammation. The authors note that most evidence comes from lab and animal studies, with limited research so far in humans.
[Environmental pollutants and Alzheimer's disease].
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