From Inhalation to Neurodegeneration: Air Pollution as a Modifiable Risk Factor for Alzheimer's Disease.
Jordi OlloquequiRoberto Diaz-PeñaEster VerdaguerMiren EtchettoCarme AuladellAntonio Camins EspunyPublished in: International journal of molecular sciences (2024)
Air pollution, a growing concern for public health, has been linked to various respiratory and cardiovascular diseases. Emerging evidence also suggests a link between exposure to air pollutants and neurodegenerative diseases, particularly Alzheimer's disease (AD). This review explores the composition and sources of air pollutants, including particulate matter, gases, persistent organic pollutants, and heavy metals. The pathophysiology of AD is briefly discussed, highlighting the role of beta-amyloid plaques, neurofibrillary tangles, and genetic factors. This article also examines how air pollutants reach the brain and exert their detrimental effects, delving into the neurotoxicity of air pollutants. The molecular mechanisms linking air pollution to neurodegeneration are explored in detail, focusing on oxidative stress, neuroinflammation, and protein aggregation. Preclinical studies, including in vitro experiments and animal models, provide evidence for the direct effects of pollutants on neuronal cells, glial cells, and the blood-brain barrier. Epidemiological studies have reported associations between exposure to air pollution and an increased risk of AD and cognitive decline. The growing body of evidence supporting air pollution as a modifiable risk factor for AD underscores the importance of considering environmental factors in the etiology and progression of neurodegenerative diseases, in the face of worsening global air quality.
Keyphrases
- air pollution
- particulate matter
- cognitive decline
- heavy metals
- induced apoptosis
- lung function
- public health
- oxidative stress
- mild cognitive impairment
- risk assessment
- cell cycle arrest
- health risk assessment
- endoplasmic reticulum stress
- traumatic brain injury
- health risk
- cerebral ischemia
- gene expression
- cell death
- copy number
- dna damage
- drinking water
- lps induced
- genome wide
- metabolic syndrome
- cell proliferation
- ischemia reperfusion injury
- neuropathic pain
- type diabetes
- inflammatory response
- cardiovascular risk factors
- binding protein
- cell therapy
- global health