Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target.

Publisher: Wiley Country of Publication: United States NLM ID: 9717231 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1099-0461 (Electronic) Linking ISSN: 10956670 NLM ISO Abbreviation: J Biochem Mol Toxicol Subsets: MEDLINE

Original Publication: New York, NY : Wiley, c1998-

Alzheimer Disease*/enzymology ; Alzheimer Disease*/etiology ; Alzheimer Disease*/pathology ; Gene Expression Regulation, Enzymologic* ; Neurotoxicity Syndromes*/enzymology ; Neurotoxicity Syndromes*/etiology ; Neurotoxicity Syndromes*/pathology; Amyloid Precursor Protein Secretases/*biosynthesis ; Aspartic Acid Endopeptidases/*biosynthesis ; Brain/*enzymology ; Environmental Exposure/*adverse effects ; Neurotoxins/*toxicity; Aged ; Animals ; Brain/pathology ; Disease Models, Animal ; Female ; Humans ; Male

Alzheimer's disease (AD) is a major public health crisis due to devastating cognitive symptoms, a lack of curative treatments, and increasing prevalence. Most cases are sporadic (>95% of cases) after the age of 65 years, implicating an important role of environmental factors in disease pathogenesis. Environmental neurotoxicants have been implicated in neurodegenerative disorders including Parkinson's Disease and AD. Animal models of AD and in vitro studies have shed light on potential neuropathological mechanisms, yet the biochemical and molecular underpinnings of AD-relevant environmental neurotoxicity remain poorly understood. Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is a potentially critical pathogenic target of environmentally induced neurotoxicity. BACE1 clearly has a critical role in AD pathophysiology: It is required for amyloid beta production and expression and activity of BACE1 are increased in the AD brain. Though the literature on BACE1 in response to environmental insults is limited, current studies, along with extensive AD neurobiology literature suggest that BACE1 deserves attention as an important neurotoxic target. Here, we critically review research on environmental neurotoxicants such as metals, pesticides, herbicides, fungicides, polyfluoroalkyl substances, heterocyclic aromatic amines, advanced glycation end products, and acrolein that modulate BACE1 and potential mechanisms of action. Though more research is needed to clearly understand whether BACE1 is a critical mediator of AD-relevant neurotoxicity, available reports provide convincing evidence that BACE1 is altered by environmental risk factors associated with AD pathology, implying that BACE1 inhibition and its use as a biomarker should be considered in AD management and research.
(© 2021 Wiley Periodicals LLC.)

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R01 ES025750 United States ES NIEHS NIH HHS; ES025750 United States ES NIEHS NIH HHS

Keywords: Alzheimer's disease; BACE1; environmental neurotoxicants; oxidative stress

0 (Neurotoxins)
EC 3.4.- (Amyloid Precursor Protein Secretases)
EC 3.4.23.- (Aspartic Acid Endopeptidases)
EC 3.4.23.46 (BACE1 protein, human)

Date Created: 20210104 Date Completed: 20210727 Latest Revision: 20220402

20231215

PMC8049945

10.1002/jbt.22694

33393683