McAfoose, Jordan, Koerner, H., and Baune, B.T. (2008) The role of TNF in aging-associated cognitive performance: a mouse model. In: Australian and New Zealand Journal of Psychiatry (42) OP083. A58-A59. From: Australasian Society for Psychiatric Research (ASPR) 2008 Annual Conference, 2-5 December 2008, Newcastle, NSW.

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Abstract

Aims: Although the age-dependent neurobiological processes leading to cognitive decline in the elderly remains to be fully understood, there is now growing evidence to suggest that age-dependent increases in pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF), might play a role in such age-associated cognitive decline. The aim of this work was to examine, using a mouse model, the effect of a deficiency of TNF (TNF−/−) on cognitive function throughout aging.

Methods: A standardized survey on cognition-like behaviour assessing learning and retention, spatial learning/memory, and cognitive flexibility was used to measure the cognitive-behavioural profile of TNF knockout and wildtype mice, across three age periods; 3, 6 and 12 months of age, respectively.

Results: All studied mice strains demonstrated successful exploration and learning processes during the training phases of the tests, which made the specific cognition like tests valid in these mice strains. In the specific cognition-like tests, the B6.TNF−/− mice demonstrated, at 3 months of age, significantly poorer learning and retention in the novel object test as compared to B6.WT mice. In addition, spatial learning and learning effectiveness were significantly poorer in B6.TNF−/− mice, at 3 months of age, as compared to B6.WT mice. While the absence of TNF was correlated with poor cognitive functioning in early adulthood, over time the deletion of TNF resulted in better cognitive performance compared to B6.WT mice.

Conclusion: Low-levels of TNF under non-inflammatory immune conditions appear essential for normal cognitive function. Moreover, the absence of TNF with age appears to protect against age-associated cognitive decline. Collectively, these findings suggest a possible role for TNF in the molecular and cellular mechanisms subserving age-related changes in learning, memory and cognition.

Item ID:	29317
Item Type:	Conference Item (Abstract / Summary)
ISSN:	1440-1614
Date Deposited:	16 Sep 2013 00:46
FoR Codes:	11 MEDICAL AND HEALTH SCIENCES > 1103 Clinical Sciences > 110319 Psychiatry (incl Psychotherapy) @ 100%
SEO Codes:	92 HEALTH > 9204 Public Health (excl. Specific Population Health) > 920410 Mental Health @ 100%
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