Amyloid-β at sublethal level impairs BDNF-induced arc expression in cortical neurons
Section snippets
Acknowledgment
This study was supported by grants from National Science Council in Taiwan (NSC-94-2320-B-037-019).
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2021, Ageing Research ReviewsCitation Excerpt :Dysfunction of the PKA/CREB pathway and subsequent genes is strongly implicated in AD etiology and can be disrupted by Aβ-dependent or independent mechanisms (Bartolotti et al., 2016; Rudy, 2020). Aβ peptides are reported to inhibit the expression of Arc and to impair BDNF-TrkB signaling (Echeverria et al., 2007; Wang et al., 2006). Some BDNF polymorphisms increase the risk for AD (Urbina-Varela et al., 2020), or might even increase the susceptibility to depression in AD patients (Borroni et al., 2009), while overexpression of TrkB is found to enhance memory (Rudy, 2020).
Rolipram-induced improvement of cognitive function correlates with changes in hippocampal CREB phosphorylation, BDNF and Arc protein levels
2016, Neuroscience LettersCitation Excerpt :Our findings suggest that rolipram supplementation of diabetic rats results in a significant increase in hippocampal Arc/Arg3.1 protein levels as well as memory and cognitive ability, an event which appears to be linked to increased BDNF and CREB activity in the hippocampus. In agreement with this, previous studies have indicated that subchronic Rolipram delivery increased the basal rat hippocampal expression and phosphorylation of CREB, as well as the expression of Arc protein [9,22]. In an exogenous BDNF-induced LTP model increased CREB activation and Arc mRNA and protein expression was simultaneously observed [36].
BONLAC: A combinatorial proteomic technique to measure stimulus-induced translational profiles in brain slices
2016, NeuropharmacologyCitation Excerpt :Finally, our comparison of BDNF-induced proteomic changes in slices versus neurons revealed that the majority of the protein candidates altered were strikingly different. Some of the changes in candidate protein abundance suggested by the neuronal culture screen had been reported previously and/or validated, supporting the findings of the BONLAC screen (Liao et al., 2009; Ying et al., 2002; Wang et al., 2006; Okuno et al., 2012). The difference between the proteomic candidates identified in neuronal cultures and those in slices are likely not due to the difference in timeframe (1-h BDNF treatment versus 2-h) as Liao et al. (2007) measured changes after 30 min of BDNF treatment.
The role of synaptic activity in the regulation of amyloid beta levels in Alzheimer's disease
2014, Neurobiology of AgingInvolvement of hippocampal Arc in amnesia and its recovery by alcoholic extract of Ashwagandha leaves
2013, Neurobiology of Learning and Memory