Topic: microgliosis

Tauopathy is a hallmark of a broad category of neurodegenerative conditions and Traumatic Brain Injury (TBI). Progression of tau pathology may lead to impaired cognitive conditions leading to dementia. However, previous studies have reported cognitively healthy patients with cortical tau pathologies. The mechanism for this cognitive protection in a tauopathy environment is being investigated by various groups. Astrocytes are essential for physiological homeostasis of brain and reactive astrogliosis is an associated pathology in neuroinflammation associated with TBI. The correlation between lev

Hypoxic-ischaemic encephalopathy (HIE) is one of the most serious complications in neonates and infants. Mesenchymal stromal cell (MSC)-based therapy is emerging as a promising treatment avenue for HIE. However, despite its enormous potential, the clinical application of MSCs is limited by cell heterogeneity, low isolation efficiency and unpredictable effectiveness. In this study, we investigated the therapeutic effects of human pluripotent stem cell-derived ectomesenchymal stromal cells (hPSC-EMSCs) and human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) in a rat model of HIE. Lesi

Metabolic disorders like diabetes and obesity markedly elevate the risk of neurodegenerative diseases. While certain medications used to manage these conditions show neuroprotective potential, their exact mechanisms of action remain elusive. Here, we propose the utilization of brain histology in a mouse prion model as an effective approach for drug screening in dementia and for exploring the cellular mechanisms of neuroprotection offered by anti-diabetic drugs. Our primary objective was to establish the morphological criteria for brain pathology in prion-infected mice. To achieve this, C57BL/6

Type 2 spastic paraplegia (SPG2) is a rare genetic disorder caused by null mutations in the gene encoding for the proteolipid protein 1, essential for myelin sheath formation around nerve fibers in the central nervous system (CNS). SPG2 manifests as progressive stiffness and weakness in the legs, accompanied by white matter abnormalities and axonal degeneration in the CNS. These myelin abnormalities impair neural communication, impacting motor function, cognition and may contribute to neuropsychological conditions like anxiety. Leriglitazone, a brain-penetrant PPARγ full agonist, has shown

X-linked dystonia-parkinsonism (XDP) is a recessive neurodegenerative disease endemic to Panay, Philippines. The XDP striatum is notably reported to undergo significant atrophy, neuronal loss, and astrogliosis. However, detailed neuropathological studies characterising the human XDP striatum are limited.To advance our understanding of the human XDP striatum, immunohistochemistry coupled with automated analysis was conducted on post-mortem striatal tissue from 12 XDP and 5 age-matched neurologically normal cases to detail (1) the neurochemical architecture and (2) neuronal and glial populations

Traumatic brain injury (TBI) is the leading cause of death in the pediatric stage, with detrimental consequences including psychosocial issues, cognitive deficits and motor abnormalities. In addition to the primary TBI impact, the subsequent neuroinflammatory response can become a contributing and even leading factor to the harmful effect of pediatric TBI on the brain. As such, finding ways to stabilize the reactive microglial phenotype is a key objective for TBI treatment. One potential factor is the neuropeptide oxytocin. Oxytocin has shown to be neuroprotective in adult neuroinflammatory st

Traumatic brain injury (TBI) is a cause of disability and a risk factor for the development of epilepsy, partially mediated by reactive gliosis. The aim of this project was to observe astroglial and microglial reactions to brain injury and identify sex differences in the process of glial scar formation.Penetrating cortical brain injury was induced on postnatal day 30 (P30) in male and female rats. The animals were perfused on P32, P38, P46, or P60. Brain tissue was sectioned and stained against glial fibrillary acidic protein (GFAP, astrocyte marker) and ionized calcium-binding adapter molecul

Obesity and metabolic disorders are linked with neurodegenerative diseases through persistent peripheral inflammation caused by metabolic alterations, which underlies chronic neuroinflammation. Pleiotrophin (PTN) is a cytokine that regulates neuroinflammation and metabolism in different contexts. Thus, our study aimed to determine the role of PTN in the brain-periphery crosstalk in a high-fat diet (HFD)-induced obesity model. Three-month-old C57BL/6J wild-type (Ptn+/+) and Ptn genetically deficient (Ptn−/−) mice were fed with standard chow diet or HFD (60% kcal fat) for 6 months. HFD-Ptn−/− mi