Literature DB >> 8229078

The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution.

B T Hyman1, K Marzloff, P V Arriagada.   

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.

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Year:  1993        PMID: 8229078     DOI: 10.1097/00005072-199311000-00006

Source DB:  PubMed          Journal:  J Neuropathol Exp Neurol        ISSN: 0022-3069            Impact factor:   3.685


  67 in total

1.  Abeta deposition is associated with neuropil changes, but not with overt neuronal loss in the human amyloid precursor protein V717F (PDAPP) transgenic mouse.

Authors:  M C Irizarry; F Soriano; M McNamara; K J Page; D Schenk; D Games; B T Hyman
Journal:  J Neurosci       Date:  1997-09-15       Impact factor: 6.167

Review 2.  Vaccines for Alzheimer's disease: how close are we?

Authors:  Christopher Janus
Journal:  CNS Drugs       Date:  2003       Impact factor: 5.749

3.  Amyloid deposition in the hippocampus and entorhinal cortex: quantitative analysis of a transgenic mouse model.

Authors:  John F Reilly; Dora Games; Russell E Rydel; Stephen Freedman; Dale Schenk; Warren G Young; John H Morrison; Floyd E Bloom
Journal:  Proc Natl Acad Sci U S A       Date:  2003-04-15       Impact factor: 11.205

4.  Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer's disease.

Authors:  T Gómez-Isla; J L Price; D W McKeel; J C Morris; J H Growdon; B T Hyman
Journal:  J Neurosci       Date:  1996-07-15       Impact factor: 6.167

Review 5.  The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

Authors:  Zi-Xuan Wang; Lan Tan; Jinyuan Liu; Jin-Tai Yu
Journal:  Mol Neurobiol       Date:  2015-04-02       Impact factor: 5.590

6.  Alzheimer-signature MRI biomarker predicts AD dementia in cognitively normal adults.

Authors:  B C Dickerson; T R Stoub; R C Shah; R A Sperling; R J Killiany; M S Albert; B T Hyman; D Blacker; L Detoledo-Morrell
Journal:  Neurology       Date:  2011-04-13       Impact factor: 9.910

Review 7.  Microglia in Alzheimer's disease.

Authors:  Heela Sarlus; Michael T Heneka
Journal:  J Clin Invest       Date:  2017-09-01       Impact factor: 14.808

8.  Serum amyloid P component prevents proteolysis of the amyloid fibrils of Alzheimer disease and systemic amyloidosis.

Authors:  G A Tennent; L B Lovat; M B Pepys
Journal:  Proc Natl Acad Sci U S A       Date:  1995-05-09       Impact factor: 11.205

9.  Quantitation of amyloid beta-protein (A beta) in the cortex during aging and in Alzheimer's disease.

Authors:  H Funato; M Yoshimura; K Kusui; A Tamaoka; K Ishikawa; N Ohkoshi; K Namekata; R Okeda; Y Ihara
Journal:  Am J Pathol       Date:  1998-06       Impact factor: 4.307

10.  A limited role for microglia in antibody mediated plaque clearance in APP mice.

Authors:  Monica Garcia-Alloza; Brian J Ferrara; Sarah A Dodwell; Gregory A Hickey; Bradley T Hyman; Brian J Bacskai
Journal:  Neurobiol Dis       Date:  2007-07-28       Impact factor: 5.996

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