Alzheimer’s disease, amyloïd peptide and synaptic dysfunction | Maladie d’Alzheimer, peptide β-amyloïde et synapses

Agnès Hémar, Christophe Mulle
Med Sci (Paris). 2011-08-01; 27(8-9): 733-736
DOI: 10.1051/medsci/2011278015

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1. Med Sci (Paris). 2011 Aug-Sep;27(8-9):733-6. doi: 10.1051/medsci/2011278015. Epub
2011 Aug 31.

[Alzheimer’s disease, amyloid peptide and synaptic dysfunction].

[Article in French]

Hémar A(1), Mulle C.

Author information:
(1)Institut interdisciplinaire de neurosciences, Université de Bordeaux, Bordeaux
Cedex, France.

Alzheimer’s disease (AD) is the first cause of dementia that leads to insidious
and progressive loss of memory and cognitive functions. In the early stages of
AD, there is a strong correlation between memory impairment and cortical levels
of soluble amyloid-β peptide oligomers (Aβ). It has become clear that Aβ disrupt
glutamatergic synaptic function, which in turn may lead to the characteristic
cognitive deficits. Conversely, experiments in rodents have conforted the notion
that Aβo impairs synaptic transmission and plasticity, and that mouse models with
increased production of these oligomers display cognitive impairment. Many
studies have attempted to determine the mechanisms by which Aβo disrupt synaptic
plasticity and mediate their detrimental effect, but the actual pathways are
still poorly understood. Here we review this thriving area of research which aims
at understanding the mechanisms of synaptic dysfunction in the early phase of AD,
and its consequences on the activity of neural circuits.

© 2011 médecine/sciences – Inserm / SRMS.

DOI: 10.1051/medsci/2011278015
PMID: 21880261 [Indexed for MEDLINE]

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