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2014 ; 111
(52
): 18733-8
Nephropedia Template TP
Pereira AC
; Lambert HK
; Grossman YS
; Dumitriu D
; Waldman R
; Jannetty SK
; Calakos K
; Janssen WG
; McEwen BS
; Morrison JH
Proc Natl Acad Sci U S A
2014[Dec]; 111
(52
): 18733-8
PMID25512503
show ga
The dementia of Alzheimer's disease (AD) results primarily from degeneration of
neurons that furnish glutamatergic corticocortical connections that subserve
cognition. Although neuron death is minimal in the absence of AD, age-related
cognitive decline does occur in animals as well as humans, and it decreases
quality of life for elderly people. Age-related cognitive decline has been linked
to synapse loss and/or alterations of synaptic proteins that impair function in
regions such as the hippocampus and prefrontal cortex. These synaptic alterations
are likely reversible, such that maintenance of synaptic health in the face of
aging is a critically important therapeutic goal. Here, we show that riluzole can
protect against some of the synaptic alterations in hippocampus that are linked
to age-related memory loss in rats. Riluzole increases glutamate uptake through
glial transporters and is thought to decrease glutamate spillover to
extrasynaptic NMDA receptors while increasing synaptic glutamatergic activity.
Treated aged rats were protected against age-related cognitive decline displayed
in nontreated aged animals. Memory performance correlated with density of thin
spines on apical dendrites in CA1, although not with mushroom spines.
Furthermore, riluzole-treated rats had an increase in clustering of thin spines
that correlated with memory performance and was specific to the apical, but not
the basilar, dendrites of CA1. Clustering of synaptic inputs is thought to allow
nonlinear summation of synaptic strength. These findings further elucidate
neuroplastic changes in glutamatergic circuits with aging and advance therapeutic
development to prevent and treat age-related cognitive decline.
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