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Age-related accumulation of Reelin in amyloid-like deposits.

Abstract：

:Accumulating evidence suggest that alterations in Reelin-mediated signaling may contribute to neuronal dysfunction associated with Alzheimer's disease (AD), the most common form of senile dementia. However, limited information is available on the effect of age, the major risk factor of AD, on Reelin expression. Here, we report that normal aging in rodents and primates is accompanied by accumulation of Reelin-enriched proteinous aggregates in the hippocampal formation that are related to the loss of Reelin-expressing neurons. Both phenomena are associated with age-related memory impairments in wild-type mice. We provide evidence that normal aging involves loss of Reelin neurons, reduced production and elimination of the extracellular deposits, whereas a prenatal immune challenge or the expression of AD-causing gene products, result in earlier, higher, and more persistent levels of Reelin-positive deposits. These aggregates co-localize with non-fibrillary amyloid-plaques, potentially representing oligomeric Abeta species. Our findings suggest that elevated Reelin plaque load creates a precursor condition for senile plaque deposition and may represent a critical risk factor for sporadic AD.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Knuesel I,Nyffeler M,Mormède C,Muhia M,Meyer U,Pietropaolo S,Yee BK,Pryce CR,LaFerla FM,Marighetto A,Feldon J

doi

10.1016/j.neurobiolaging.2007.08.011

subject

Has Abstract

pub_date

2009-05-01 00:00:00

pages

697-716

issue

5

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(07)00338-7

journal_volume

30

pub_type

杂志文章

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