AGE

, Volume 35, Issue 3, pp 583–596

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Authors

  • Zhiqian Tong
    • State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of SciencesGraduate University of the Chinese Academy of Sciences
  • Chanshuai Han
    • State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of SciencesGraduate University of the Chinese Academy of Sciences
  • Wenhong Luo
    • Central LaboratoryShantou University Medical College
  • Xiaohui Wang
    • Department of Neurobiology and National Key Discipline of PhysiologyShanxi Medical University
  • Hui Li
    • Central LaboratoryShantou University Medical College
  • Hongjun Luo
    • Central LaboratoryShantou University Medical College
  • Jiangning Zhou
    • University of Science and Technology of China
    • Department of Neurobiology and National Key Discipline of PhysiologyShanxi Medical University
    • State Key Laboratory of Brain and Cognitive Sciences, Institute of BiophysicsChinese Academy of Sciences
    • Key Lab of Mental Health, Institute of PsychologyChinese Academy of Sciences
Article

DOI: 10.1007/s11357-012-9388-8

Cite this article as:
Tong, Z., Han, C., Luo, W. et al. AGE (2013) 35: 583. doi:10.1007/s11357-012-9388-8

Abstract

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.

Keywords

Alzheimer’s disease (AD)AgingEndogenous formaldehydeLong-term potentiation (LTP)Long-term memory (LTM)NMDA receptor

Copyright information

© American Aging Association 2012