Age-related structural changes in the rat hippocampus: correlation with working memory deficiency
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Social housing protects against age-related working memory decline independently of physical enrichment in rats
2019, Neurobiology of AgingCitation Excerpt :WM is a limited capacity system that holds short-term information in support of an individual task, whereas RM holds long-term memories acquired with repeated exposure to a certain task. These age-related impairments, particularly in WM, are disruptive to overall quality of life because they can appear as early as middle age and are observed in both spatial and nonspatial domains (Bizon et al., 2009; Bopp and Verhaeghen, 2005; Frick et al., 1995; Kadar et al., 1990; Lester et al., 2017; Lindner et al., 1992; Pitsikas and Algeri, 1992; Wang et al., 2011; Wyss et al., 2000). Identifying how specific lifestyle factors impact WM is imperative, especially considering that WM disruptions may be predictive of disease-related decline (Summers and Saunders, 2012) and are thought to be a mechanism for decline in higher order cognition (Bopp and Verhaeghen, 2005; Salthouse, 1994; Salthouse et al., 1991).
Loss of CB1 receptors leads to decreased cathepsin D levels and accelerated lipofuscin accumulation in the hippocampus
2013, Mechanisms of Ageing and DevelopmentCitation Excerpt :Cathepsin D expression and intracellular distribution are also known to be affected by aging (Nakanishi, 2003). Although lipofuscin accumulation is often considered to be just an aging marker, many studies have shown that it often accompanies cellular degeneration and inflammatory processes (Cai et al., 2012; Ma et al., 2013; Shiozaki et al., 2008), as well as cognitive decline during aging (Kadar et al., 1990). Lipofuscin is considered to be the major source of oxidants in aging cells (Hohn et al., 2010).
Vacuolation and mineralisation as dominant age-related findings in hamster brains
2013, Experimental and Toxicologic PathologyCitation Excerpt :Clinically, a mild accumulation of lipofuscin in the cell seems to be without deleterious effect. A deposition of lipofuscin, especially in the CA3 region of the hippocampus was associated with an age-dependent cognitive decline in dogs and rats (Borràs et al., 1999; Kadar et al., 1990). The large area of necrosis and gliosis in the CA1 region of the hippocampus of one animal was most likely caused by an infarction with scar formation due to the selective vulnerability of hippocampal CA1 pyramidal cells to ischemic lesions (Ordy et al., 1993).
What do we know about aging and spatial cognition? Reviews and perspectives
2012, Ageing Research ReviewsCitation Excerpt :Moreover, plasticity (i.e., long term potentialization) at perforant synapses has been shown to be deficient in aged rats with poor spatial memory (Barnes and McNaughton, 1985; Barnes, 1979). Finally, decreases in neuron density in the pyramidal cell fields of the hippocampus have been found to be most pronounced in aged rats with spatial learning impairment (Kadar et al., 1990; Jiang et al., 1989). Overall, models of age-related spatial learning impairment have revealed that a combination of many hippocampal changes (i.e., connectivity and plasticity) may contribute to the observed age-related allocentric spatial learning decline in rodents.