Behavioral Neurobiology of Aging by Kathleen M. Hayden, Kathleen A. Welsh-Bohmer (auth.),

By Kathleen M. Hayden, Kathleen A. Welsh-Bohmer (auth.), Marie-Christine Pardon, Mark W. Bondi (eds.)

This quantity discusses the present kingdom of study findings regarding fit mind getting older through integrating human medical stories and translational study in animal versions. numerous chapters provide a distinct review of profitable getting older, age-related cognitive decline and its linked structural and practical mind alterations, in addition to how those alterations are inspired through reproductive getting older. Insights supplied by way of preclinical stories in mouse versions and complex neuroimaging innovations in people also are presented.

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Data from the CCS suggested a possible explanation because apparent benefits were observed only among participants who reported use of both water-soluble vitamin (C) and lipid-soluble vitamin E, but not among users of either vitamin alone (Zandi et al. 2004). More recent analyses of cognitive decline in CCMS cognitive screening scores from Waves I–IV again found a suggestive reduction in ‘‘normal’’ age-related cognitive decline in users of both vitamins, but neither alone (Wengreen et al. 2007).

Acta Neurol Scand Suppl 165:3–12 Brayne C, Stephan BC et al (2011) A European perspective on population studies of dementia. Alzheimers Dement 7(1):3–9 Epidemiology of Cognitive Aging and Alzheimer’s Disease 27 Breitner JC, Gau BA et al (1994a) Inverse association of anti-inflammatory treatments and Alzheimer’s disease: initial results of a co-twin control study. Neurology 44(2):227–232 Breitner JC, Welsh KA et al (1994b) Alzheimer’s disease in the NAS-NRC registry of aging twin veterans. II. Longitudinal findings in a pilot series.

Starting NSAID use after age 65 may actually have the opposite effect and act to accelerate AD symptom onset. The mechanism for these disparate effects of NSAIDS on AD expression is unclear but may be related to brain inflammatory mechanisms widely thought to influence AD pathogenesis (Weggen et al. 2001). In the extended presymptomatic period of AD neurodegeneration, NSAID use may act to suppress brain inflammatory response and delay AB deposition. However, once AB deposition is already in process, the brain inflammatory response may be crucial to AB clearance (Martin et al.

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