Topic: ADAM10

Development of pro-neurogenic therapies for compensating the neuronal loss and restoration of degenerated synaptic networks in neurodegenerative diseases has been difficult to achieve, which calls for new strategies to promote adult neurogenesis and counteract neurodegeneration. BRI2 is a ubiquitously expressed transmembrane protein that undergoes proteolytic processing, resulting in the formation of several secreted peptides. The precise physiological function of BRI2 remains elusive, however preliminary results suggested an increase in BRI2 levels during neuronal development, and a strong ph

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

Oligodendrocytes, the myelinating glial cells of the central nervous system (CNS), surround axons with their membrane extensions, forming the myelin sheath. Loss of oligodendrocytes and/or myelin (demyelination) occurs in traumatic brain injury or pathologies such as multiple sclerosis. Since, there is no specific treatment for demyelination; we are interested in enhancing myelin endogenous repair. We focus our work on A Disintegrin and Metalloprotease (ADAM) 10, the major CNS α-secretase, which generates the neuroprotective soluble fragment sAPPα via cleavage of the Amyloid Precursor Protein

Ageing has been defined as a gradual functional decline with a progressive physiological integrity loss, increasing the organism’s vulnerability to death. Otherwise, this described deterioration is the major risk factor for most current human pathologies, including neurodegenerative diseases, cancer, cardiovascular disorders, and diabetes. However, in the last decades, non-pharmacological treatments like physical exercise have provided general health benefits against ageing decline. In this study, we aim to analyze how lifestyle factors such as physical exercise can modify the molecular expres