Literature DB >> 8434881

Synapse loss in the temporal lobe in Alzheimer's disease.

S W Scheff1, D A Price.   

Abstract

The temporal lobe is a well-documented area showing neuropathological and neurochemical changes in Alzheimer's disease (AD). Autopsy tissue was obtained from the superior temporal (Brodmann area 22) and the middle temporal (Brodmann area 21) regions of the cortex from patients with AD (n = 10; postmortem time < 13 hr) and age-matched control subjects (n = 10; postmortem time < 13 hr). Ultrastructural examination of the tissue revealed a highly significant AD-related decline in synaptic numbers in lamina III and V in both the superior and the middle temporal gyrus. Both normal control and AD tissue samples demonstrated a significant negative correlation between the number of synapses and the synapse size, as indexed by the length of the postsynaptic density. This change in synaptic size appears to compensate for the loss of synaptic numbers when viewed in terms of total synaptic contact area. Although the AD tissue showed an average 30% decline in synaptic numbers, the total synaptic contact area remained largely unchanged in both regions of the cortex. There were no significant correlations with age, postmortem time, or number of plaques observed in these areas. The loss of synaptic contacts in AD does not appear to be isolated to a particular cortical region or lamina.

Entities:  

Mesh:

Year:  1993        PMID: 8434881     DOI: 10.1002/ana.410330209

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  76 in total

1.  Staging of cytoskeletal and beta-amyloid changes in human isocortex reveals biphasic synaptic protein response during progression of Alzheimer's disease.

Authors:  E B Mukaetova-Ladinska; F Garcia-Siera; J Hurt; H J Gertz; J H Xuereb; R Hills; C Brayne; F A Huppert; E S Paykel; M McGee; R Jakes; W G Honer; C R Harrington; C M Wischik
Journal:  Am J Pathol       Date:  2000-08       Impact factor: 4.307

Review 2.  Impaired regulation of synaptic actin cytoskeleton in Alzheimer's disease.

Authors:  Peter Penzes; Jon-Eric Vanleeuwen
Journal:  Brain Res Rev       Date:  2011-01-26

3.  Reactive synaptogenesis in aging and Alzheimer's disease: lessons learned in the Cotman laboratory.

Authors:  Stephen Scheff
Journal:  Neurochem Res       Date:  2003-11       Impact factor: 3.996

4.  Involvement of perineuronal and perisynaptic extracellular matrix in Alzheimer's disease neuropathology.

Authors:  Markus Morawski; Gert Brückner; Carsten Jäger; Gudrun Seeger; Russel T Matthews; Thomas Arendt
Journal:  Brain Pathol       Date:  2012-01-13       Impact factor: 6.508

5.  Flexible modulation of network connectivity related to cognition in Alzheimer's disease.

Authors:  Donald G McLaren; Reisa A Sperling; Alireza Atri
Journal:  Neuroimage       Date:  2014-05-20       Impact factor: 6.556

Review 6.  Amyotrophic lateral sclerosis: current and future treatment strategies.

Authors:  B W Festoff
Journal:  Drugs       Date:  1996-01       Impact factor: 9.546

7.  Neurofibrillary tangle predominant form of senile dementia of Alzheimer type: a rare subtype in very old subjects.

Authors:  C Bancher; K A Jellinger
Journal:  Acta Neuropathol       Date:  1994       Impact factor: 17.088

8.  Cell death in Alzheimer's disease evaluated by DNA fragmentation in situ.

Authors:  H Lassmann; C Bancher; H Breitschopf; J Wegiel; M Bobinski; K Jellinger; H M Wisniewski
Journal:  Acta Neuropathol       Date:  1995       Impact factor: 17.088

Review 9.  Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer's disease Neurons.

Authors:  Ravi Rajmohan; P Hemachandra Reddy
Journal:  J Alzheimers Dis       Date:  2017       Impact factor: 4.472

Review 10.  Pathogenesis of synaptic degeneration in Alzheimer's disease and Lewy body disease.

Authors:  Cassia R Overk; Eliezer Masliah
Journal:  Biochem Pharmacol       Date:  2014-01-21       Impact factor: 5.858

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.