Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation.
Aging
/ genetics
Aluminum
/ toxicity
Alzheimer Disease
/ etiology
Amyloid beta-Peptides
/ genetics
Animals
Cadmium
/ toxicity
Disease Models, Animal
Environmental Exposure
/ adverse effects
Gene Expression Regulation
/ drug effects
Humans
Inflammation
Lead
/ toxicity
Life Style
Physical Fitness
Presenilin-1
/ genetics
tau Proteins
/ genetics
dementia
environment
neurodegeneration
tau
β-amyloid
Journal
Journal of molecular biology
ISSN: 1089-8638
Titre abrégé: J Mol Biol
Pays: Netherlands
ID NLM: 2985088R
Informations de publication
Date de publication:
19 04 2019
19 04 2019
Historique:
received:
01
11
2018
revised:
10
01
2019
accepted:
11
01
2019
pubmed:
22
1
2019
medline:
20
3
2020
entrez:
22
1
2019
Statut:
ppublish
Résumé
As the median age of the population increases, the number of individuals with Alzheimer's disease (AD) and the associated socio-economic burden are predicted to worsen. While aging and inherent genetic predisposition play major roles in the onset of AD, lifestyle, physical fitness, medical condition, and social environment have emerged as relevant disease modifiers. These environmental risk factors can play a key role in accelerating or decelerating disease onset and progression. Among known environmental risk factors, chronic exposure to various metals has become more common among the public as the aggressive pace of anthropogenic activities releases excess amount of metals into the environment. As a result, we are exposed not only to essential metals, such as iron, copper, zinc and manganese, but also to toxic metals including lead, aluminum, and cadmium, which perturb metal homeostasis at the cellular and organismal levels. Herein, we review how these metals affect brain physiology and immunity, as well as their roles in the accumulation of toxic AD proteinaceous species (i.e., β-amyloid and tau). We also discuss studies that validate the disruption of immune-related pathways as an important mechanism of toxicity by which metals can contribute to AD. Our goal is to increase the awareness of metals as players in the onset and progression of AD.
Identifiants
pubmed: 30664867
pii: S0022-2836(19)30027-0
doi: 10.1016/j.jmb.2019.01.018
pmc: PMC6475603
mid: NIHMS1519074
pii:
doi:
Substances chimiques
Amyloid beta-Peptides
0
MAPT protein, human
0
PSEN1 protein, human
0
Presenilin-1
0
tau Proteins
0
Cadmium
00BH33GNGH
Lead
2P299V784P
Aluminum
CPD4NFA903
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1843-1868Subventions
Organisme : NIEHS NIH HHS
ID : R01 ES024331
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.
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