Topic: chronic neuroinflammation

Chronic neuroinflammation, associated with central nervous system (CNS) pathologies, involves persistent microglial activation. Misfolded proteins in Alzheimer’s disease and mechanical CNS lesions initiate prolonged immune responses, contributing to neuronal damage. Recent literature suggests the induction of controlled immune modulation to foster neuro-restoration. We propose the use of protein kinase C (PKC) activators to modulate CNS innate immune cells (i.e., microglia) for regenerative therapeutic approaches. Therefore, we examined the molecular and functional effect of PKC activators (Pr

Heat shock proteins (HSPs) are evolutionarily conserved chaperones. Previously our group observed that overexpression of HSPB1 improved certain symptoms of Alzheimer’s disease (AD) in mice. The primary role of these chaperons is to maintain the protein homeostasis, however, several evidence suggest that they have additional functions, such as regulating inflammation. Therefore, our aim is to investigate the role of HSPB1 in chronic neuroinflammation and glia activation in a mouse model of AD.AD model (APP/PS1) mouse strain was crossed with an HSPB1 overexpressing line. Expression pattern of HS

The human APOE4 genotype has been identified as a crucial risk factor for developing neurodegenerative diseases, such as Alzheimer, in elderly. However, no clear directions to generate a prevention plan for APOEε4 carriers exist nowadays. In this sense, current knowledge states that chronic neuroinflammation is a convergent point to neural diseases, contributing to neurodegeneration. Interestingly, APOE is an immunomodulatory agent, establishing a nexus between those premises. However, mechanisms underlying this association are yet to be clarified.We aimed to identify in aged transgenic mice t