Scientific Reports - Persistent open chromatin state in early-life stress-activated cells of the VTA

CRISPR-based tools can’t easily access the DNA in these organelles, but researchers are finding other ways in.

Alzheimer's disease (AD) has traditionally been associated with amyloid-β plaques, but growing evidence underscores the role of neuroinflammation in disease progression. The autoinflammatory hypothesi...

Remyelination, the process by which axons are re-encased in myelin after injury, is a critical step in restoring brain function, yet the dynamics from initial injury to repair remain poorly characteri...

Serino et al. show that seeing an infectious avatar approach the body in virtual reality triggers an immune response, indicating that the brain prepares the body to fight infections even for perceived...

In this Resource paper, the authors use MIBI spatial proteomics to map microglial cell states in brains from cognitively normal humans and those with Alzheimer’s disease.

Microglia-mediated neuroinflammation drives Alzheimer's disease (AD) pathogenesis, yet the underlying mechanism is poorly understood. Song et al. demonstrate that toxic amyloid-β induces oxidation and...

imageimageGlia activation, inflammation, cell death pathways and neuronal pathologies are associated with disease progression in preclinical AD. Activation of glia cells and cell death pathways mainta...

The announcement of the first phase of the ceasefire in Gaza brings a welcome moment of relief for exhausted, starved and grieving Palestinians and a great relief to the families of all hostages — but...

Scientists have identified an unusual type of brain cell that may play a vital role in progressive multiple sclerosis (MS), likely contributing to the persistent inflammation characteristic of the dis...

Stroke is a major cause of disability. Astrocytes respond to stroke in a gradated manner, but details of that response and its consequences for tissue…

Neuroinflammation in the pathogenesis of neurodegenerative diseases is still a subject of discussion, as it might be either the cause or the result of neurodegeneration. Misfolded or improperly aggregated α-synuclein in Parkinson’s Disease, can cause inflammatory responses, indicating a mechanistic relationship between α-synuclein pathology and neuroinflammation. The aim of this study was to investigate the role of DNA topoisomerase IIβ, the key player of DNA topology, in the neuroinflammation process in an age-dependent transgenic Parkinson’s Disease mouse model overexpressing the A53T mutant α-synuclein. In this study, transgenic and control mice were bred in three age groups as early (3 months), mid (8 months), and late (12 months) disease stages. Behavioral experiments were carried out to compare the age-related cognitive and motor coordination functions. Cytokine levels in the serum and protein expression levels in the dissected brain were analyzed by both western blot and immunofluorescence staining. A decline was observed in the cognitive and motor coordination functions depending on age. Disease-related markers at protein level appeared even in the early stage, and accordingly, a significant increase was observed in inflammatory markers and cytokine levels compared to control. DNA Topoisomerase IIβ and Nurr1 levels decreased in transgenic mice, especially more dramatically in the early stage. The combined effect of reduced Nurr1 and DNA Topoisomerase IIβ, along with increased inflammation, may provide a better understanding of the pathogenesis of Parkinson’s Disease at early-stage and requires for further investigation of the potential alterations in topo IIβ as an intervention strategy for this disease.

Activity in a set of parabranchial neurons in the mouse brain is increased during chronic pain, predicts coping behaviour, and can be modulated by circuits activated by survival threats.