The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Neuroinflammation in Alzheimer's disease and prion disease
Abstract
Alzheimer's disease (AD) and prion disease are characterized neuropathologically by extracellular deposits of Aβ and PrP amyloid fibrils, respectively. In both disorders, these cerebral amyloid deposits are co‐localized with a broad variety of inflammation‐related proteins (complement factors, acute‐phase protein, pro‐inflammatory cytokines) and clusters of activated microglia. The present data suggest that the cerebral Aβ and PrP deposits are closely associated with a locally induced, non‐immune‐mediated chronic inflammatory response. Epidemiological studies indicate that polymorphisms of certain cytokines and acute‐phase proteins, which are associated with Aβ plaques, are genetic risk factors for AD. Transgenic mice studies have established the role of amyloid associated acute‐phase proteins in Alzheimer amyloid formation. In contrast to AD, there is a lack of evidence that cytokines and acute‐phase proteins can influence disease progression in prion disease. Clinicopathological and neuroradiological studies have shown that activation of microglia is a relatively early pathogenetic event that precedes the process of neuropil destruction in AD patients. It has also been found that the onset of microglial activation coincided in mouse models of prion disease with the earliest changes in neuronal morphology, many weeks before neuronal loss and subsequent clinical signs of disease. In the present work, we review the similarities and differences between the involvement of inflammatory mechanisms in AD and prion disease. We also discuss the concept that the demonstration of a chronic inflammatory‐like process relatively early in the pathological cascade of both diseases suggests potential therapeutic strategies to prevent or to retard these chronic neurodegenerative disorders. GLIA 40:232–239, 2002. © 2002 Wiley‐Liss, Inc.
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Citations
Cites
Inflammation and Alzheimer’s disease
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Cited by
Immune attack: the role of inflammation in Alzheimer disease
Heppner, F. L., Ransohoff, R. M., & Becher, B. (2015) · Nature Reviews Neuroscience · doi:10.1038/nrn3880 · Cited by 2,134
Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism
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Inflammation in neurodegenerative diseases
Amor, S., Puentes, F., Baker, D., & Van Der Valk, P. (2010) · Immunology · doi:10.1111/j.1365-2567.2009.03225.x · Cited by 1,355
Impairment of Glymphatic Pathway Function Promotes Tau Pathology after Traumatic Brain Injury
Iliff, J. J., Chen, M. J., Plog, B. A., Zeppenfeld, D. M., Soltero, M., Yang, L., Singh, I., Deane, R., & Nedergaard, M. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.3020-14.2014 · Cited by 1,159
Three or more routes for leukocyte migration into the central nervous system
Ransohoff, R. M., Kivisäkk, P., & Kidd, G. (2003) · Nature Reviews Immunology · doi:10.1038/nri1130 · Cited by 1,052
Metadata
- Authors
- Eikelenboom, P., Bate, C., Van Gool, W. A., Hoozemans, J. J. M., Rozemuller, J. M., Veerhuis, R., & Williams, A.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2002-10-04
- Volume
- 40
- Issue
- 2
- Pages
- 232-239
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2089701069
- Cited by
- 405
- References
- 63
- FWCI
- 11.72
- Type
- journal article
- Language
- en
- Open access
- closed
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- Eikelenboom, P., Bate, C., Van Gool, W. A., Hoozemans, J. J. M., Rozemuller, J. M., Veerhuis, R., & Williams, A. (2002). Neuroinflammation in Alzheimer's disease and prion disease. Glia. https://doi.org/10.1002/glia.10146
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