Our website is made possible by displaying online advertisements to our visitors.
Please consider supporting us by disabling your ad blocker.
Amyloid plaques
Amyloid plaques (also known as neuritic plaques, amyloid beta plaques or senile plaques) are extracellular deposits of amyloid beta (Aβ) protein that present mainly in the grey matter of the brain.[1][2][3][4] Degenerative neuronal elements and an abundance of microglia and astrocytes can be associated with amyloid plaques. Some plaques occur in the brain as a result of aging, but large numbers of plaques and neurofibrillary tangles are characteristic features of Alzheimer's disease.[5] The plaques are highly variable in shape and size; in tissue sections immunostained for Aβ, they comprise a log-normal size distribution curve, with an average plaque area of 400-450 square micrometers (μm2). The smallest plaques (less than 200 μm2), which often consist of diffuse deposits of Aβ,[4] are particularly numerous.[6] Plaques form when Aβ misfolds and aggregates into oligomers and longer polymers, the latter of which are characteristic of amyloid.[7]
- ^ Cras P; Kawai M; Lowery D; Gonzalez-DeWhitt P; Greenberg B; Perry G (September 1991). "Senile plaque neurites in Alzheimer disease accumulate amyloid precursor protein". Proceedings of the National Academy of Sciences of the United States of America. 88 (17): 7552–6. Bibcode:1991PNAS...88.7552C. doi:10.1073/pnas.88.17.7552. PMC 52339. PMID 1652752.
- ^ Purves, Dale; Augustine, George J.; Fitzpatrick, David; Hall, William C.; LaManita, Anthony-Samuel; White, Leonard E.; Mooney, Richard D.; Platt, Michael L. (2012). Neuroscience (5th ed.). Sunderland, MA: Sinauer Associates. p. 713. ISBN 978-0-87893-695-3.
- ^ Dickson DW (1997). "The pathogenesis of senile plaques". J Neuropathol Exp Neurol. 56 (4): 321–339. doi:10.1097/00005072-199704000-00001. PMID 9100663.
- ^ a b Walker LC (2020). "Aβ plaques". Free Neuropathology. 1 (31): 31. doi:10.17879/freeneuropathology-2020-3025. PMC 7745791. PMID 33345256.
- ^ Ballard, C; Gauthier, S; Corbett, A; Brayne, C; Aarsland, D; Jones, E (19 March 2011). "Alzheimer's disease". Lancet. 377 (9770): 1019–31. doi:10.1016/S0140-6736(10)61349-9. PMID 21371747. S2CID 20893019.
- ^ Hyman BT; West HL; Rebeck GW; Buldyrev SV; Mantegna RN; Ukleja M; Havlin S; Stanley HE (1995). "Quantitative analysis of senile plaques in Alzheimer disease: observation of log-normal size distribution and molecular epidemiology of differences associated with apolipoprotein E genotype and trisomy 21 (Down syndrome)". Proceedings of the National Academy of Sciences of the United States of America. 92 (8): 3586–3590. Bibcode:1995PNAS...92.3586H. doi:10.1073/pnas.92.8.3586. PMC 42212. PMID 7724603.
- ^ Röhr D, Boon BD, Schuler M, et al. (December 2020). "Label-free vibrational imaging of different Aβ plaque types in Alzheimer's disease reveals sequential events in plaque development". Acta Neuropathologica Communications. 8 (1): 222. doi:10.1186/s40478-020-01091-5. PMC 7733282. PMID 33308303.
Previous Page Next Page
