Amyloid β and Alzheimer’s Disease: Molecular Updates from Physiology to Pathology
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: closed (15 January 2021) | Viewed by 6857
Special Issue Editor
Interests: Alzheimer’s disease; molecular neurobiology; amyloid-β; primary cortical neurons; signal transduction; BDNF; insulin and insulin-like growth factor signaling in Alzheimer's disease; HSP60; Aβ and copper; small molecules and peptide inhibitors of Aβ aggregation
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear colleagues,
Alzheimer’s disease (AD) is still an incurable disease with an incidence that is expected to increase in the near future. In previous decades, the pathophysiology of AD has been extensively investigated. Several approaches have been employed to disclose the molecular mechanisms underlying the cellular dysfunctions typically observed in AD. From in vitro and in vivo findings, we have learned that Aβ oligomers (AβOs), rather than Aβ fibrils, are mainly responsible for the effects leading to neurodegeneration. They have shown a better correlation with the severity of the disease and, in line with this observation, were found to induce synaptic dysfunction in the early stage of the disease, promote oxidative stress, and interfere with the activation of important cellular receptors. However, besides these unquestionable roles of Aβ oligomers, the primary cause of Aβ over-production and aggregation is far from being completely clarified.
Moreover, after initial evidence that Aβ monomers are innocuous, an increasing amount of data have indicated that Aβ may have important physiological roles in neuronal activity. A more comprehensive understanding of Aβ functions, from physiology to the occurrence of AD pathological conditions, could contribute to the refinement of pharmacological interventions and the design of new drug candidates.
Most AD drugs have been projected to block Aβ production or aggregation. However, the targeting of all Aβ species, including monomers, might be the reason for the continuous failure of clinical trials. The recent encouraging results of antibodies which preferentially bind to toxic AβOs seem to support this view.
The aim of this Special Issue of IJMS is to collect, in a broader perspective, scientific papers as well as reviews of the current literature, that deal with amyloid beta peptide function in health and/or disease. All original works that look at the role of Aβ within and beyond the disease and contribute to the improvement of the molecular understanding of Alzheimer’s disease are welcome.
Dr. Maria Laura Giuffrida
Guest Editor
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Keywords
- Alzheimer’s disease
- Aβ monomers
- Aβ oligomers
- signal transduction
- neuroprotection
- anti- Aβ therapy
