Amyloid-β activity in neuronal physiology and Alzheimer’s disease Pathology
The research activity is focused on molecular mechanisms involved in Alzheimer’s disease (AD) progression with particular attention to the role of Amyloid-beta (Aβ) in both physiological/pre-clinical conditions and AD pathology.
The research activity is focused on the understanding of the molecular mechanisms underlying physiological and pathological processes involved in the arising of Alzheimer’s disease (AD). In particular, the study aims to clarify the still debated role of Amyloid-beta (Aβ) peptide in normal neuronal physiology and all the mechanisms leading to its aggregation, a condition linked to AD pathology. To investigate Aβ functions as a monomeric peptide or differently sized aggregated species, molecular and cellular approaches are routinely used. Pure cortical neurons or mixed glial/neuronal cells are prepared from rat embryos to have reliable cellular models to be used for this research. In the past few years, within this field of interest, the study of the molecular mechanisms shared between Alzheimer’s and Type II Diabetes has been also deepened, leading to interesting implications in the identification of new potential targets of AD therapy.
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-Giuffrida ML, Tomasello MF, Pandini G, Caraci F, Battaglia G, Busceti C, Di Pietro P, Pappalardo G, Attanasio F, Chiechio S, Bagnoli S, Nacmias B, Sorbi S, Vigneri R, Rizzarelli E, Nicoletti F, Copani A.(2015) Monomeric ß-amyloid interacts with type-1 insulin-like growth factor receptors to provide energy supply to neurons. Front Cell Neurosci. Aug 7;9:297. doi: 10.3389/fncel.2015.00297.
-Zimbone S, Monaco I, Giani F, Pandini G, Copani AG, Giuffrida ML, Rizzarelli E (2018). Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type-1 insulin-like growth factor receptors in neuronal cells. Aging Cell. ISSN: 1474-9726. vol. 17, ISSN: 1474-9726, doi: 10.1111/acel.12684.
