Association Between Particulate Matter and Alzheimer’s Disease in Elderly Subjects

Alzheimer’s disease (AD) is a type of dementia, which causes memory, thinking, and behavior associated problem. AD symptoms develop slowly and along with time it progressed into chronic condition. In fact, it interferes with routine activities. The lifestyle, genetics, and environmental factors are major precursors of AD. However, exact cause of AD is still unknown.

The combustion of fossil fuel releases particulate matter (PM) in air. PM are fusion of solid and liquid particle suspended in air. This fusion includes both organic and inorganic particles such as pollen, liquid droplets, soot, and dust. Most of these PMs are hazardous. People often exposed to these matters and develops Alzheimer’s.

Research

Increasing AD incidence with accompanying cognitive decline and memory loss posts serious economic, social and health delivery problems at a global scale. Studies have indicated that air pollution, largely caused by increasing urbanization and may be of etiologic importance. After going through various studies showing a possible relationship between PM and AD, the research tested the hypothesis that an association exists between exposure to PM and AD. Air pollution containing PM, ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and lead is largely found in urban atmosphere. In this review paper my focus is on ambient air PM.  Several studies have demonstrated the ability of PM to cross the blood-brain barrier and reach the CNS. However, PM may also reach the brain through the systemic circulation. This paper explores the relationship between ambient air PM and AD in elderly subjects in order to learn whether AD may be, to some extent, a preventable disease.

Our literature review on Alzheimer’s disease have presented findings indicating that ambient air PM is associated with AD. The fine (PM2.5) and ultra-fine (PM0.1) particles seems to carry the greatest risk to the CNS. Individuals exposed to high levels of ambient air pollution experiences inflammatory responses and brain damage similar to AD, in frontal cortex, olfactory mucosa and olfactory bulb. Ambient air PM may reach the brain through either the nasal pathway or through the lungs via the systemic circulation. Small size PM may be able to reach the brain easily to produce oxidative stress by releasing cytokines. Ambient air PM may also be involved in producing ROS, which may result in formation of amyloid beta peptides and senile plaques surrounded by neurofibrillary tangles similar to AD. Since accumulation of amyloid-beta42 may be accelerated by air pollution, and exposure to ambient air PM are associated with impaired cognitive function, a plausible association exists between PM and AD.

Provided ambient air pollution is an etiologic factor, AD may at least partly be a preventable condition depending on the ability to reduce air pollution, especially in heavy populated areas. More research is needed to learn more about the risk factors and mechanisms involved in the genesis of AD according to ambient air PM. If ambient air pollution is causally related to AD, the Public Health sectors need to work closely with communities, organizations, states and federal authorities to increase awareness of the problem, and to propose policy changes to minimize exposure.

“Rearch by Dr. Nasira Tajamal”