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
. 2009 Jan-Mar;3(1):88-93.
doi: 10.4161/cam.3.1.7402. Epub 2009 Jan 13.

Oxidative stress in Alzheimer disease

Alejandro Gella  1 , Nuria Durany
Affiliations
Review

Oxidative stress in Alzheimer disease

Alejandro Gella et al. Cell Adh Migr. 2009 Jan-Mar.

Abstract

Alzheimer disease (AD) is a progressive dementia affecting a large proportion of the aging population. The histopathological changes in AD include neuronal cell death, formation of amyloid plaques and neurofibrillary tangles. There is also evidence that brain tissue in patients with AD is exposed to oxidative stress (e.g., protein oxidation, lipid oxidation, DNA oxidation and glycoxidation) during the course of the disease. Advanced glycation endproducts (AGEs) are present in amyloid plaques in AD, and its extracellular accumulation may be caused by an accelerated oxidation of glycated proteins. AGEs participate in neuronal death causing direct (chemical) and indirect (cellular) free radical production and consequently increase oxidative stress. The development of drugs for the treatment of AD that breaks the vicious cycles of oxidative stress and neurodegeneration offer new opportunities. These approaches include AGE-inhibitors, antioxidants and anti-inflammatory substances, which prevent free radical production.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Sources and effects of oxidative stress on a molecular and cellular level.
Figure 2
Figure 2
Chemical reactions leading to the formation of advanced glycation endproducts.
Figure 3
Figure 3
Direct and indirect effects of advanced glycation endproducts through crosslinking of Aβ peptide.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Gsell W, Strein I, Riederer P. The neurochemistry of Alzheimer type, vascular type and mixed type dementias compared. J Neural Transm. 1996;47:73–101. - PubMed
    1. Gsell W, Strein I, Krause U, Riederer P. Neurochemical abnormalities in Alzheimer's disease and Parkinson's disease—a comparative review. J Neural Transm. 1997;51:145–159. - PubMed
    1. Retz W, Gsell W, Münch G, Rosler M, Riederer P. Free radicals in Alzheimer's disease. J Neural Transm. 1998;54:221–236. - PubMed
    1. Rösler M, Retz W, Thome J, Riederer P. Free radicals in Alzheimer's dementia: currently available therapeutic strategies. J Neural Transm. 1998;54:211–219. - PubMed
    1. Durany N, Münch G, Michel T, Riederer P. Investigations on oxidative stress and therapeutical implications in dementia. Eur Arch Psychiatry Clin Neurosci. 1999;249:68–73. - PubMed