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Early detection of memory deficits and memory improvement with vaccinia virus complement control protein in an Alzheimer's disease model.
Behav Brain Res 2008; 192(2):173-7BB

Abstract

Vaccinia virus complement control protein (VCP) inhibits both the classical and alternate complement pathways. In diseases such as traumatic brain injury (TBI) and Alzheimer's disease (AD), pathological inflammation is caused by amongst several factors, prolonged or inappropriate activation of the complement system and is a significant cause of neurodegeneration. This study investigates for the first time the use of a cheeseboard maze to evaluate cognitive deficits and the effect of VCP on memory processes in 2- and 3-month-old mice that express mutant amyloid precursor protein (APPswe) and mutant presenilin 1 (Ps1dE9) that correspond to a form of early onset AD. A four-phase training schedule was carried out on the cheeseboard maze before intracranial injections of 5 microl of VCP (1.7 microg/microl) or 5 microl saline. Two weeks later the effect of VCP on memory was evaluated. A statistically significant decrease in goal latency in VCP-treated mice than saline-treated transgenic mice in both the first probe and reverse tasks was observed. Similarly, after a second intracranial VCP or saline injection performed 2 months later, the 6.5- and 7.5-month aged VCP-injected mice performed significantly better in goal latency in both second probe and reverse tasks than saline-treated mice. These data also demonstrated that the use of a dry maze is a sensitive technique for distinguishing cognitive measures between non-transgenic and APPswe/PS1De9 transgenic mice at a much earlier stage.

Authors+Show Affiliations

Division of Medical Virology, South Africa.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

18490064

Citation

Pillay, Nirvana S., et al. "Early Detection of Memory Deficits and Memory Improvement With Vaccinia Virus Complement Control Protein in an Alzheimer's Disease Model." Behavioural Brain Research, vol. 192, no. 2, 2008, pp. 173-7.
Pillay NS, Kellaway LA, Kotwal GJ. Early detection of memory deficits and memory improvement with vaccinia virus complement control protein in an Alzheimer's disease model. Behav Brain Res. 2008;192(2):173-7.
Pillay, N. S., Kellaway, L. A., & Kotwal, G. J. (2008). Early detection of memory deficits and memory improvement with vaccinia virus complement control protein in an Alzheimer's disease model. Behavioural Brain Research, 192(2), pp. 173-7. doi:10.1016/j.bbr.2008.03.038.
Pillay NS, Kellaway LA, Kotwal GJ. Early Detection of Memory Deficits and Memory Improvement With Vaccinia Virus Complement Control Protein in an Alzheimer's Disease Model. Behav Brain Res. 2008 Oct 10;192(2):173-7. PubMed PMID: 18490064.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early detection of memory deficits and memory improvement with vaccinia virus complement control protein in an Alzheimer's disease model. AU - Pillay,Nirvana S, AU - Kellaway,Laurie A, AU - Kotwal,Girish J, Y1 - 2008/04/07/ PY - 2007/11/19/received PY - 2008/03/27/revised PY - 2008/03/31/accepted PY - 2008/5/21/pubmed PY - 2008/10/1/medline PY - 2008/5/21/entrez SP - 173 EP - 7 JF - Behavioural brain research JO - Behav. Brain Res. VL - 192 IS - 2 N2 - Vaccinia virus complement control protein (VCP) inhibits both the classical and alternate complement pathways. In diseases such as traumatic brain injury (TBI) and Alzheimer's disease (AD), pathological inflammation is caused by amongst several factors, prolonged or inappropriate activation of the complement system and is a significant cause of neurodegeneration. This study investigates for the first time the use of a cheeseboard maze to evaluate cognitive deficits and the effect of VCP on memory processes in 2- and 3-month-old mice that express mutant amyloid precursor protein (APPswe) and mutant presenilin 1 (Ps1dE9) that correspond to a form of early onset AD. A four-phase training schedule was carried out on the cheeseboard maze before intracranial injections of 5 microl of VCP (1.7 microg/microl) or 5 microl saline. Two weeks later the effect of VCP on memory was evaluated. A statistically significant decrease in goal latency in VCP-treated mice than saline-treated transgenic mice in both the first probe and reverse tasks was observed. Similarly, after a second intracranial VCP or saline injection performed 2 months later, the 6.5- and 7.5-month aged VCP-injected mice performed significantly better in goal latency in both second probe and reverse tasks than saline-treated mice. These data also demonstrated that the use of a dry maze is a sensitive technique for distinguishing cognitive measures between non-transgenic and APPswe/PS1De9 transgenic mice at a much earlier stage. SN - 0166-4328 UR - https://www.unboundmedicine.com/medline/citation/18490064/Early_detection_of_memory_deficits_and_memory_improvement_with_vaccinia_virus_complement_control_protein_in_an_Alzheimer's_disease_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(08)00182-4 DB - PRIME DP - Unbound Medicine ER -