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2013 ; 35
(3
): 583-96
Nephropedia Template TP
Tong Z
; Han C
; Luo W
; Wang X
; Li H
; Luo H
; Zhou J
; Qi J
; He R
Age (Dordr)
2013[Jun]; 35
(3
): 583-96
PMID22382760
show ga
Aging is an important factor in memory decline in aged animals and humans and in
Alzheimer's disease and is associated with the impairment of hippocampal
long-term potentiation (LTP) and down-regulation of NR1/NR2B expression. Gaseous
formaldehyde exposure is known to induce animal memory loss and human cognitive
decline; however, it is unclear whether the concentrations of endogenous
formaldehyde are elevated in the hippocampus and how excess formaldehyde affects
LTP and memory formation during the aging process. In the present study, we
report that hippocampal formaldehyde accumulated in memory-deteriorating diseases
such as age-related dementia. Spatial memory performance was gradually impaired
in normal Sprague-Dawley rats by persistent intraperitoneal injection with
formaldehyde. Furthermore, excess formaldehyde treatment suppressed the
hippocampal LTP formation by blocking N-methyl-D-aspartate (NMDA) receptor.
Chronic excess formaldehyde treatment over a period of 30 days markedly decreased
the viability of the hippocampus and down-regulated the expression of the NR1 and
NR2B subunits of the NMDA receptor. Our results indicate that excess endogenous
formaldehyde is a critical factor in memory loss in age-related
memory-deteriorating diseases.