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Research Article Pages 105-112
Abstract: Alzheimer's disease (AD) is a global public health crisis. Currently, there are no treatments to prevent or halt the disease. Given the precedence of chronic neuroinflammation in triggering AD-like neurodegeneration and an observed upregulation of NFkB-driven miRs i.e. mir-125b positively correlating with AD, silencing specific micro-RNA with antisense-microRNA (antagomir) to miR-125b was undertaken to evaluate its efficacy in ameliorating AD-like neurodegeneration in 5XFAD transgenic mice modeling AD.
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Research Article Pages 99-104
Abstract: Anti-tau immunotherapies targeting phospho-epitopes have shown promising outcome in pre-clinical studies, although, with certain limitations in terms of mode of antibody delivery and concentration of antibodies required to obtain positive outcome.
Research Article Pages 92-98
Abstract: Soluble oligomers of amyloid-beta peptide (Abeta) have been implicated in the onset of memory deficits in Alzheimer’s disease, perhaps due to their reported ability to impair long-term potentiation (LTP) of synaptic strength. We previously showed the effect of Abeta on LTP depends on the strength of LTP induction. Furthermore, Abeta affects EPSP-Spike (E-S) potentiation more robustly than LTP, suggesting that E-S potentiation may be equally important to learning and memory in the context of Alzheimer’s disease.
Research Article Pages 85-91
Abstract: Both Alzheimer’s disease (AD) and HIV-associated neurocognitive disorders (HAND) could progress to dementia, a severe consequence of neurodegenerative diseases. Cumulating evidence suggests that the β-amyloid (Aβ) theory, currently thought to be the predominant mechanism underlying AD and AD-related dementia (ADRD), needs re-evaluation, considering all treatments and new drug trials based upon this theory have been unsuccessful.
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