Hostname: page-component-848d4c4894-p2v8j Total loading time: 0.001 Render date: 2024-05-21T06:03:42.832Z Has data issue: false hasContentIssue false
  • English
  • Français

Microscopic Evaluation of Oxidative Damage in Alzheimer Disease

Published online by Cambridge University Press:  02 July 2020

M. A. Smith  and
G. Perry
M. A. Smith
Affiliation:
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH, 44106
G. Perry
Affiliation:
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH, 44106
Get access

Extract

In the past five years, a case for oxidative stress in the pathogenesis of Alzheimer disease (AD) has been convincingly made. That link owes most of its existence to the microscopic detection of neuronal oxidative damage. Focusing on damage not only has the advantage that stable products are studied, rather than short-lived radicals, but also that damage can be morphologically defined. This latter aspect is critical since biochemical analysis of whole tissue is mostly of the accumulated damage from normal metabolism with aging of long-lived polymers in the extracellular matrix (Figure 1). The importance of damage is that it is the result most likely to be linked to pathology. Driven by the hypothesis that oxidative damage plays a role in the aggregation of insoluble protein in the lesions of Alzheimer disease, neurofibrillary tangles and senile plaques, we developed reagents to detect protein modifications related to glycoxidation, lipid peroxidation, peroxynitrite, free carbonyls and carbonyl-modification (Figure 2).

Type
Application of Novel Microscopic Approaches To Cellular Damage and Response
Information
Microscopy and Microanalysis , Volume 3 , Issue S2: Proceedings: Microscopy & Microanalysis '97, Microscopy Society of America 55th Annual Meeting, Microbeam Analysis Society 31st Annual Meeting, Histochemical Society 48th Annual Meeting, Cleveland, Ohio, August 10-14, 1997 , August 1997 , pp. 41 - 42
Copyright
Copyright © Microscopy Society of America 1997

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Smith, M. A.et al., Brain Res. 717(1996)99–108.10.1016/0006-8993(95)01473-XCrossRefGoogle Scholar
2.Smith, M. A.et al., Proc. Natl. Acad. Sci., USA 91 (1994)5710–5714.10.1073/pnas.91.12.5710CrossRefGoogle Scholar
3.Yan, S. -D.et al., Proc. Natl. Acad. Sci, USA 91(1994)7787–7791.10.1073/pnas.91.16.7787CrossRefGoogle Scholar
4.Sayre, L. M.et al., J. Neurochem. 68( 1997)2092–2097.10.1046/j.1471-4159.1997.68052092.xCrossRefGoogle Scholar
5.Smith, M. A.et al., J. Neurosci. 17(1997) in press.Google Scholar
6.Smith, M. A.et al., Nature 382(1996)120–121.10.1038/382120b0CrossRefGoogle Scholar
7.Smith, M. A.et al., J. Neurochem. 64(1995)2660–2666.10.1046/j.1471-4159.1995.64062660.xCrossRefGoogle Scholar
8.Smith, M. A.et al., Am. J. Pathol. 145 (1994)42–47.Google Scholar
9.Yan, S. D.et al., Nature Medicine 1 (1995)693–699.10.1038/nm0795-693CrossRefGoogle Scholar
10.Premkumar, D. R. D.et al., J. Neurochem. 65(1995)1399–1402.10.1046/j.1471-4159.1995.65031399.xCrossRefGoogle Scholar
11.Praprotnik, D.et al., Acta Neuropathol 91(1996)1–5.10.1007/s004010050385CrossRefGoogle Scholar
12.Praprotnik, D.et al., Acta Neuropathol 91(1996)226–235.10.1007/s004010050420CrossRefGoogle Scholar
13.Smith, M. A., Perry, G., Alzheimer's Disease Review 1(1996)63–67.Google Scholar
14.Smith, M. A.et al., Neurosci. Lett. 217(1996)210–211.10.1016/0304-3940(96)13100-1CrossRefGoogle Scholar
15. This work was supported by the National Institutes of Health (AG09287) and the American Health Assistance Foundation.Google Scholar