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2022, Ageing Research ReviewsCitation Excerpt :The cellular and molecular mechanisms underlying synaptic plasticity and cognitive functions mediated by p75NTR in aging and several age-related neurodegenerative diseases (Table 1) is discussed in more details in the following sections. Synaptic plasticity and cognitive functions are known to be affected during aging (Deupree et al., 1991; Wong et al., 2021; Barnes et al., 2000b). A number of studies have found that the expression of p75NTR during normal aging is increased in different brain regions, including the hippocampus (Costantini et al., 2005; Terry Jr et al., 2011; Wong et al., 2021; Vanguilder Starkey et al., 2013), prefrontal cortex (Terry Jr et al., 2011) and basal forebrain (Fortress et al., 2011).
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2022, Neurochemistry InternationalCitation Excerpt :Rather, it appears that age-related cognitive decline is mediated through the alterations in synaptic number and function in brain regions responsible for memory-related tasks, such as the hippocampus or prefrontal cortex (Burke and Barnes, 2006; Morrison and Baxter, 2012). Aged animals show either a higher threshold for LTP induction (Barnes et al., 2000) or a decreased level of LTP induction compared with young animals (Barnes et al., 2000; Deupree et al., 1991; Tombaugh et al., 2002). In addition, LTP maintenance is decreased in the dentate gyrus and CA3 of aged rats (Dieguez and Barea-Rodriguez, 2004), and LTP observed in these animals is more susceptible to depotentiation (Norris et al., 1996).
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2017, Brain Research BulletinSecreted amyloid precursor protein-alpha can restore novel object location memory and hippocampal LTP in aged rats
2017, Neurobiology of Learning and MemoryCitation Excerpt :A dose-response analysis would be needed to test this hypothesis, although this is beyond the scope of the current study. During aging, LTP induction and maintenance are susceptible to age-related impairments (Barnes, 1979; Deupree, Turner, & Watters, 1991; Kumar & Foster, 2004; Landfield et al., 1978). We found that sAPPα delivered to hippocampal slices had no effect on basal synaptic transmission or paired-pulse plasticity, but completely rescued LTP in slices from aged rats to the level seen in untreated slices from young rats.