Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015:2015:515248.
doi: 10.1155/2015/515248. Epub 2015 Nov 17.

Alzheimer's Disease: Exploring the Role of Inflammation and Implications for Treatment

Affiliations
Review

Alzheimer's Disease: Exploring the Role of Inflammation and Implications for Treatment

Mark E McCaulley et al. Int J Alzheimers Dis. 2015.

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by both structural abnormalities and inflammation in the brain. While recent research has chiefly focused on the structural changes involved in AD, understanding the pathophysiology and associated inflammation of the AD brain helps to elucidate potential therapeutic and preventative options. By exploring the data supporting an inflammatory etiology of AD, we present a case for the use of existing evidence-based treatments addressing inflammation as promising options for treating and preventing AD. We present data demonstrating tumor necrosis factor alpha association with the inflammation of AD. We also discuss data supporting TNF alpha associated inflammation in traumatic brain injury, stroke, and spinal disc associated radiculopathy. We augment this previously unarticulated concept of a unifying pathophysiology of central nervous system disease, with reports of benefits of TNF alpha inhibition in many hundreds of patients with those diseases, including AD. We also assess the pathophysiologic and clinical trial evidence supporting the role of other inflammation resolving treatments in AD. In aggregate, the data from the several potentially effective therapeutic and preventative options contained within this report presents a clearer picture of next steps needed in research of treatment alternatives.

PubMed Disclaimer

References

    1. Morris G. P., Clark I. A., Vissel B. Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease. Acta Neuropathologica Communications. 2014;2(1, article 135) doi: 10.1186/s40478-014-0135-5. - DOI - PMC - PubMed
    1. Drachman D. A. The amyloid hypothesis, time to move on: amyloid is the downstream result, not cause, of Alzheimer's disease . Alzheimer's and Dementia. 2014;10(3):372–380. doi: 10.1016/j.jalz.2013.11.003. - DOI - PubMed
    1. Ishii T., Haga S., Shimizu F. Identification of components of immunoglobulins in senile plaques by means of fluorescent antibody technique. Acta Neuropathologica. 1975;32(2):157–162. doi: 10.1007/bf00689569. - DOI - PubMed
    1. Ishii T., Haga S. Immuno-electron-microscopic localization of complements in amyloid fibrils of senile plaques. Acta Neuropathologica. 1984;63(4):296–300. doi: 10.1007/bf00687336. - DOI - PubMed
    1. Fillit H., Ding W., Buee L., et al. Elevated circulating tumor necrosis factor levels in Alzheimer's disease. Neuroscience Letters. 1991;129(2):318–320. doi: 10.1016/0304-3940(91)90490-k. - DOI - PubMed