Topic: amyloid-ß peptide

Neurodegenerative disorders, such as Alzheimer’s disease (AD), are the object of intense investigation due to their prevalence worldwide and the lack of an effective treatment to mitigate cognitive deterioration. This is because we still do not fully understand what triggers sporadic AD although several risk factors that predisposed disease development have been identified. Among them, genetic variants of the Apolipoprotein E (ApoE) or gene mutations in ADAM10 or TREM2 proteins have attracted particular attention, either for their prevalence and/or their relationship to glial cell function. In

Alzheimer’s disease (AD) has wide-ranging health and economical impact affecting millions globally. The molecular mechanisms behind AD are not yet understood, but alterations in the processing and clearance of Amyloid precursor protein (APP), such as increased levels of specific APP fragments like Amyloid-ß peptide (Aß), have been observed in early-stage AD. Increased Aß concentration leads to impaired long-term potentiation (LTP) at hippocampal CA1-CA3 synapses, the process that can be restored by partially blocking GluN2B-NMDA receptor (Ronicke et al., Neurobiol. Aging 2011). We modeled comp