Tags

Type your tag names separated by a space and hit enter

Glucocorticoids increase impairments in learning and memory due to elevated amyloid precursor protein expression and neuronal apoptosis in 12-month old mice.
Eur J Pharmacol. 2010 Feb 25; 628(1-3):108-15.EJ

Abstract

Alzheimer's disease is a chronic neurodegenerative disorder marked by a progressive loss of memory and cognitive function. Stress level glucocorticoids are correlated with dementia progression in patients with Alzheimer's disease. In this study, twelve month old male mice were chronically treated for 21 days with stress-level dexamethasone (5mg/kg). We investigated the pathological consequences of dexamethasone administration on learning and memory impairments, amyloid precursor protein processing and neuronal cell apoptosis in 12-month old male mice. Our results indicate that dexamethasone can induce learning and memory impairments, neuronal cell apoptosis, and mRNA levels of the amyloid precursor protein, beta-secretase and caspase-3 are selectively increased after dexamethasone administration. Immunohistochemistry demonstrated that amyloid precursor protein, caspase-3 and cytochrome c in the cortex and CA1, CA3 regions of the hippocampus are significantly increased in 12-month old male mice. Furthermore, dexamethasone treatment induced cortex and hippocampus neuron apoptosis as well as increasing the activity of caspase-9 and caspase-3. These findings suggest that high levels of glucocorticoids, found in Alzheimer's disease, are not merely a consequence of the disease process but rather play a central role in the development and progression of Alzheimer's disease. Stress management or pharmacological reduction of glucocorticoids warrant additional consideration of the regimen used in Alzheimer's disease therapies.

Authors+Show Affiliations

Department of Pharmacology, Anhui Medical University, Hefei, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19948164

Citation

Li, Wei-Zu, et al. "Glucocorticoids Increase Impairments in Learning and Memory Due to Elevated Amyloid Precursor Protein Expression and Neuronal Apoptosis in 12-month Old Mice." European Journal of Pharmacology, vol. 628, no. 1-3, 2010, pp. 108-15.
Li WZ, Li WP, Yao YY, et al. Glucocorticoids increase impairments in learning and memory due to elevated amyloid precursor protein expression and neuronal apoptosis in 12-month old mice. Eur J Pharmacol. 2010;628(1-3):108-15.
Li, W. Z., Li, W. P., Yao, Y. Y., Zhang, W., Yin, Y. Y., Wu, G. C., & Gong, H. L. (2010). Glucocorticoids increase impairments in learning and memory due to elevated amyloid precursor protein expression and neuronal apoptosis in 12-month old mice. European Journal of Pharmacology, 628(1-3), 108-15. https://doi.org/10.1016/j.ejphar.2009.11.045
Li WZ, et al. Glucocorticoids Increase Impairments in Learning and Memory Due to Elevated Amyloid Precursor Protein Expression and Neuronal Apoptosis in 12-month Old Mice. Eur J Pharmacol. 2010 Feb 25;628(1-3):108-15. PubMed PMID: 19948164.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucocorticoids increase impairments in learning and memory due to elevated amyloid precursor protein expression and neuronal apoptosis in 12-month old mice. AU - Li,Wei-Zu, AU - Li,Wei-Ping, AU - Yao,Yu-You, AU - Zhang,Wen, AU - Yin,Yan-Yan, AU - Wu,Guo-Cui, AU - Gong,Hui-Ling, Y1 - 2009/12/02/ PY - 2009/06/05/received PY - 2009/10/19/revised PY - 2009/11/03/accepted PY - 2009/12/2/entrez PY - 2009/12/2/pubmed PY - 2010/4/7/medline SP - 108 EP - 15 JF - European journal of pharmacology JO - Eur. J. Pharmacol. VL - 628 IS - 1-3 N2 - Alzheimer's disease is a chronic neurodegenerative disorder marked by a progressive loss of memory and cognitive function. Stress level glucocorticoids are correlated with dementia progression in patients with Alzheimer's disease. In this study, twelve month old male mice were chronically treated for 21 days with stress-level dexamethasone (5mg/kg). We investigated the pathological consequences of dexamethasone administration on learning and memory impairments, amyloid precursor protein processing and neuronal cell apoptosis in 12-month old male mice. Our results indicate that dexamethasone can induce learning and memory impairments, neuronal cell apoptosis, and mRNA levels of the amyloid precursor protein, beta-secretase and caspase-3 are selectively increased after dexamethasone administration. Immunohistochemistry demonstrated that amyloid precursor protein, caspase-3 and cytochrome c in the cortex and CA1, CA3 regions of the hippocampus are significantly increased in 12-month old male mice. Furthermore, dexamethasone treatment induced cortex and hippocampus neuron apoptosis as well as increasing the activity of caspase-9 and caspase-3. These findings suggest that high levels of glucocorticoids, found in Alzheimer's disease, are not merely a consequence of the disease process but rather play a central role in the development and progression of Alzheimer's disease. Stress management or pharmacological reduction of glucocorticoids warrant additional consideration of the regimen used in Alzheimer's disease therapies. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/19948164/Glucocorticoids_increase_impairments_in_learning_and_memory_due_to_elevated_amyloid_precursor_protein_expression_and_neuronal_apoptosis_in_12_month_old_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(09)01094-2 DB - PRIME DP - Unbound Medicine ER -