Aging brain

About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.

Genetic aberrancies and neurodegenerative disorders

Abstract: Contents. List of Contributors. Preface (M.P. Mattson and J.W. Geddes). Toward a Cognitive Neuroscience of Normal Aging (P.R. Rapp and M. Gallagher). The Neuronal Cytoskeleton: Changes Associated with Age, Neurodegenerative Disease, and Neuronal Insult (J.W. Geddes and A.I. Matus). Structural Changes in the Aged Brain (D.W. Dickson). Cerebrovascular Changes in the Aging Brain (J.C. de la Torre). Metabolism of the Aging Brain (J.P. Blass, G.E. Gibson, and S. Hoyer). Contribution of Mitochondrial Alterations to Brain Aging (G. Benzi and A. Moretti). Protein Oxidation Processes in Aging Brain (D.A. Butterfield and E.R. Stadtman). Neuroendocrine Aspects of the Aging Brain (P.M. Wise, J.P. Herman, and P.W. Landfield). Changes in Neurotransmitter Signal Transduction Pathways in the Aging Brain (J.F. Kelly and G.S. Roth). Food Restriction and Brain Aging (C.E. Finch and T.E. Morgan). Neurotrophic Factors and the Aging Brain (M.P. Mattson and O. Lindvall). Index.

Assessment of neuroinflammation in the aging hippocampus using large-molecule microdialysis: Sex differences and role of purinergic receptors.

Abstract: Aging is associated with an enhanced neuroinflammatory response to acute immune challenge, often termed “inflammaging.” However, there are conflicting reports about whether baseline levels of inflammatory markers are elevated under ambient conditions in the aging brain, or whether such changes are observed predominantly in response to acute challenge. The present studies utilized two distinct approaches to assess inflammatory markers in young and aging Fischer 344 rats. Experiment 1 examined total tissue content of inflammatory markers from hippocampus of adult (3 month), middle-aged (12 month), and aging (18 month) male Fischer (F) 344 rats using multiplex analysis (23-plex). Though trends emerged for several cytokines, no significant differences in basal tissue content were observed across the 3 ages examined. Experiment 2 measured extracellular concentrations of inflammatory factors in the hippocampus from adult (3 month) and aging (18 month) males and females using large-molecule in vivo microdialysis. Although few significant aging-related changes were observed, robust sex differences were observed in extracellular concentrations of CCL3, CCL20, and IL-1α. Experiment 2 also evaluated the involvement of the P2X7 purinergic receptor in neuroinflammation using reverse dialysis of the selective agonist BzATP. BzATP produced an increase in IL-1α and IL-1β release and rapidly suppressed the release of CXCL1, CCL2, CCL3, CCL20, and IL-6. Other noteworthy sex by aging trends were observed in CCL3, IL-1β, and IL-6. Together, these findings provide important new insight into late-aging and sex differences in neuroinflammation, and their regulation by the P2X7 receptor.

Aging enhances intracerebral hemorrhage-induced brain injury in rats.

Abstract: Age is an important factor affecting oxidative stress and plasticity after brain injury. The present study investigated the effects of aging on brain injury after intracerebral hemorrhage (ICH). Aging (18- month) and young (3-month) male Sprague-Dawley rats received an intracerebral infusion of 100-µl autologous blood. Age-related changes in brain edema and neurological deficits were examined and heat shock protein 27 (HSP27) and heat shock protein 32 (HSP32) levels were determined by Western blotting. Perihematomal brain swelling was more severe in aged rats compared to young rats at three days after ICH (P < 0.05). The behavioral tests used were forelimb placing test and forelimb use asymmetry test. There were more severe neurological deficits and a slower recovery in aged rats compared to those in young rats after ICH (P < 0.05). In addition, perihematomal HSP27 and HSP32 protein levels were higher (p < 0.05) in aged rats. In conclusion, ICH causes more severe brain swelling and neurological deficits in aged rats. Clarification of the mechanisms of brain injury after ICH in the aging brain should help develop new therapeutic strategies for hemorrhagic brain injury.