Vasefi Maryam, Ghaboolian-Zare Ehsan, Abedelwahab Hamzah, Osu Anthony
Department Biology, Lamar University, Beaumont, TX, United States.
Department Biology, Lamar University, Beaumont, TX, United States.
Neurochem Int. 2020 Dec;141:104852. doi: 10.1016/j.neuint.2020.104852. Epub 2020 Sep 30.
Alzheimer's disease (AD) is the most common form of dementia, which causes progressive memory loss and cognitive decline. Effective strategies to treat or prevent remains one of the most challenging undertakings in the medical field. AD is a complex and multifactorial disease that involves several risk factors. Aging and genetic factors both play important roles in the onset of the AD, however; certain environmental factors have been reported to increase the risk of AD. Chronic exposure to toxins has been seen as an environmental factor that may increase the risk of developing a neurodegenerative disease such as AD. Exposure to metals and biotoxins produced by bacteria, molds, and viruses may contribute to the cognitive decline and pathophysiology associated with AD. Toxins may contribute to the pathology of the disease through various mechanisms such as deposition of amyloid-beta (Aβ) plaques and tangles in the brain, induction of apoptosis, inflammation, or oxidative damage. Here, we will review how toxins affect brain physiology with a focus on mechanisms by which toxins may contribute to the development and progression of AD. A better understanding of these mechanisms may help contribute towards the development of an effective strategy to slow the progression of AD.
阿尔茨海默病（AD）是最常见的痴呆形式，会导致进行性记忆丧失和认知衰退。治疗或预防AD的有效策略仍然是医学领域最具挑战性的任务之一。AD是一种复杂的多因素疾病，涉及多种风险因素。然而，衰老和遗传因素在AD的发病中都起着重要作用；据报道，某些环境因素会增加患AD的风险。长期接触毒素被视为一种可能增加患神经退行性疾病（如AD）风险的环境因素。接触细菌、霉菌和病毒产生的金属和生物毒素可能导致与AD相关的认知衰退和病理生理变化。毒素可能通过多种机制导致疾病病理，如大脑中β-淀粉样蛋白（Aβ）斑块和缠结的沉积、诱导细胞凋亡、炎症或氧化损伤。在此，我们将重点回顾毒素如何影响大脑生理，特别是毒素可能导致AD发生和发展的机制。更好地理解这些机制可能有助于制定有效的策略来减缓AD的进展。
