Skip to main content
Full access
LETTER
Published Online: 1 October 2008

Arsenic Exposure May Be a Risk Factor for Alzheimer’s Disease

Publication: The Journal of Neuropsychiatry and Clinical Neurosciences
To the Editor: Alzheimer’s disease is a progressive neurodegenerative disease, manifested by cognitive and memory deficits that impair daily activities and cause a variety of psychiatric and behavioral disturbances. 1 Many risk factors have been proposed, which, due to some cellular and subcellular mechanisms, finally lead to brain nerve apoptosis.
In Alzheimer’s disease, signs of inflammation of microglia and astroglia are present inside and outside amyloid deposits. It has been shown that there is a relationship between inflammation, reduction of neuronal functions, and deposition of amyloid. In addition, epidemiological studies have shown that anti-inflammatory drugs could reduce the risk of Alzheimer’s disease. 2
The p38 mitogen activated protein kinase (p38 MAPK) is a stress-activated enzyme responsible for transducing inflammatory signals and initiating apoptosis. The activation of this kinase is associated with neuritic plaques and neurofibrillary tangles. 2 The c-Jun N -terminal kinase 3 (JNK3) causes tau phosphorylation and finally leads to the formation of neurofibrillary tangles. 3 The neuritic plaques and neurofibrillary tangles are involved in the pathogenesis of Alzheimer’s disease.
Arsenic and its compounds are used in pesticides, insecticides, herbicides, and some kinds of alloys. Non-occupational sources of arsenic include contaminated food, water, air, and cigarette smoking. 4, 5
Workers in industries that use or produce arsenic or arsenic compounds are at risk of exposure. Consumers can be exposed to arsenic or arsenic compounds in the air from production and processing facilities, such as copper and lead smelters, wood treatment plants, and coal burning power plants. Consumers may also be exposed to arsenic or arsenic compounds when using consumer products such as pesticides, fungicides, weed killers, preserved wood, and wood treatment products. If wood that has been treated is burned in a fireplace or wood-burning stove, it is possible to create acute toxic levels of arsenic products in the air of the home.
Arsenic can induce apoptosis in cortical neurons of rats. This process is based on the activation of JNK3 and p38 MAPK by arsenic. 5 According to above-mentioned information, arsenic can activate the p38 MAPK and JNK3, which may cause brain neuronal apoptosis and lead to Alzheimer’s disease. Therefore, using protective masks and improving work atmospheric conditions are necessary for reducing the exposure to this environmental hazard.

References

1.
Cummings JL: Alzheimer’s disease. N Engl J Med 2004; 351:56–67
2.
Hull M, Lieb K, Fiebich BL: Pathways of inflammatory activation in Alzheimer’s disease: potential targets for disease modifying drugs. Curr Med Chem 2002; 9:83–88
3.
Sato S, Tatebayashi Y, Akagi T, et al: Aberrant tau phosphorylation by glycogen synthase kinase-3beta and JNK3 induces oligomeric tau fibrils in COS-7 cells. J Biol Chem 2002; 277:42060–42065
4.
American Conference of Governmental Industrial Hygienists (ACGIH®): Documentation of the arsenic, elemental and inorganic compounds (except arsine) TLV, in Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, Ohio, ACGIH Worldwide, 2003
5.
Namgung U, Xia Z: Arsenic induces apoptosis in rat cerebellar neurons via activation of JNK3 and p38 MAP kinases. Toxicol Appl Pharmacol 2001; 174:130–138

Information & Authors

Information

Published In

Go to The Journal of Neuropsychiatry and Clinical Neurosciences
Go to The Journal of Neuropsychiatry and Clinical Neurosciences
The Journal of Neuropsychiatry and Clinical Neurosciences
Pages: 501
PubMed: 19196946

History

Published online: 1 October 2008
Published in print: Fall, 2008

Authors

Details

Shahriar Gharibzadeh, M.D., Ph.D.
Biomedical Engineering Faculty, Amirkabir University of Technology, Somayyeh, Hafez, Tehran, Iran
Sayed Shahabuddin Hoseini, M.D.
Medical Sciences/University of Tehran, Iran

Metrics & Citations

Metrics

Citations

Export Citations

If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download.

For more information or tips please see 'Downloading to a citation manager' in the Help menu.

Format
Citation style
Style
Copy to clipboard

View Options

View options

PDF/EPUB

View PDF/EPUB

Get Access

Login options

Already a subscriber? Access your subscription through your login credentials or your institution for full access to this article.

Personal login Institutional Login Open Athens login
Purchase Options

Purchase this article to access the full text.

PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences

PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences

Not a subscriber?

Subscribe Now / Learn More

PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development.

Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.).

Media

Figures

Other

Tables

Share

Share

Share article link

Share