The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution
- PMID: 8229078
- DOI: 10.1097/00005072-199311000-00006
The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution
Abstract
A beta, a nearly insoluble peptide, is generally assumed to irreversibly deposit and accumulate as senile plaques (SP) during the course of Alzheimer's disease (AD). We have studied temporal neocortex of normal elderly subjects, AD patients, and elderly Down syndrome (DS) patients to determine whether A beta accumulates with age or with increasing duration of illness. We measured the number, size distribution, and total area (amyloid burden) of A beta immunoreactive deposits using computerized image analysis techniques. We found far fewer SP in normal control subjects than in AD patients, who in turn have fewer SP than elderly DS patients. No measure of A beta correlated with age in the control subjects, nor duration of illness in AD or DS patients. These data indicate that A beta may not continue to accumulate during these disease processes and support the view that the amount of A beta observed at autopsy may reflect competing processes of deposition and resolution of amyloid.
Similar articles
-
Sequence of deposition of heterogeneous amyloid beta-peptides and APO E in Down syndrome: implications for initial events in amyloid plaque formation.Neurobiol Dis. 1996 Feb;3(1):16-32. doi: 10.1006/nbdi.1996.0003. Neurobiol Dis. 1996. PMID: 9173910
-
Mostly separate distributions of CLAC- versus Abeta40- or thioflavin S-reactivities in senile plaques reveal two distinct subpopulations of beta-amyloid deposits.Am J Pathol. 2004 Jul;165(1):273-81. doi: 10.1016/s0002-9440(10)63295-6. Am J Pathol. 2004. PMID: 15215182 Free PMC article.
-
Alzheimer's disease amyloid-beta links lens and brain pathology in Down syndrome.PLoS One. 2010 May 20;5(5):e10659. doi: 10.1371/journal.pone.0010659. PLoS One. 2010. PMID: 20502642 Free PMC article.
-
Alzheimer's disease.Subcell Biochem. 2012;65:329-52. doi: 10.1007/978-94-007-5416-4_14. Subcell Biochem. 2012. PMID: 23225010 Review.
-
[Elucidating Pathogenic Mechanisms of Early-onset Alzheimer's Disease in Down Syndrome Patients].Yakugaku Zasshi. 2017;137(7):801-805. doi: 10.1248/yakushi.16-00236-2. Yakugaku Zasshi. 2017. PMID: 28674290 Review. Japanese.
Cited by
-
Examining the diagnostic value of the mnemonic discrimination task for classification of cognitive status and amyloid-beta burden.Neuropsychologia. 2023 Dec 15;191:108727. doi: 10.1016/j.neuropsychologia.2023.108727. Epub 2023 Nov 7. Neuropsychologia. 2023. PMID: 37939874 Free PMC article.
-
Different effects of constitutive and induced microbiota modulation on microglia in a mouse model of Alzheimer's disease.Acta Neuropathol Commun. 2020 Jul 29;8(1):119. doi: 10.1186/s40478-020-00988-5. Acta Neuropathol Commun. 2020. PMID: 32727612 Free PMC article.
-
Exploring a mathematical model for the kinetics of beta-amyloid molecular imaging probes through a critical analysis of plaque pathology.Mol Imaging Biol. 2006 May-Jun;8(3):151-62. doi: 10.1007/s11307-006-0037-4. Mol Imaging Biol. 2006. PMID: 16552500
-
Inflammation and Alzheimer's disease.Neurobiol Aging. 2000 May-Jun;21(3):383-421. doi: 10.1016/s0197-4580(00)00124-x. Neurobiol Aging. 2000. PMID: 10858586 Free PMC article. Review.
-
Alzheimer-signature MRI biomarker predicts AD dementia in cognitively normal adults.Neurology. 2011 Apr 19;76(16):1395-402. doi: 10.1212/WNL.0b013e3182166e96. Epub 2011 Apr 13. Neurology. 2011. PMID: 21490323 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical