The work adds to a growing body of evidence suggesting that schizophrenia and certain other neuropsychiatric conditions may be in part neuroinflammatory disorders.

Summary: People with schizophrenia and other neuropsychiatric disorders may have a more permissive blood-brain barrier which allows the immune system to become more actively involved in the central nervous system. The resulting inflammation may contribute to the clinical manifestation of psychosis-like symptoms.

Source: University of Pennsylvania

Like a stern bodyguard for the central nervous sytem, the blood-brain barrier keeps out anything that could lead to disease and dangerous inflammation–at least when all is functioning normally.

That may not be the case in people with schizophrenia and other mental disorders, suggest new findings from a team led by researchers from the School of Veterinary Medicine, Perelman School of Medicine, and Children’s Hospital of Philadelphia (CHOP).

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In this study we aimed to generate mouse antibodies against epitopes found on NPCs. We isolated one antibody (NSC-6) and characterized it in detail. Mass spectrometry using human hippocampal tissue revealed the identity of the recognized antigen as BASP1, a signaling protein that plays a key role in neurite outgrowth and plasticity^{14,15,16,17,18,19}, but here, we demonstrate that it might be utilized as a marker of NSCs in the adult brain.

Similar approaches to developing antibodies against mouse embryonic stem cells have been attempted in the past utilizing mice^46,47 and rabbits⁴⁸. Major drawbacks in mice include immune tolerance to mouse embryonic stem cell surface antigens leading to low antibody production, which could be overcome by immunizing rabbits instead. Regardless of the animal used as a host, a significant number of antibodies are typically generated against intracellular epitopes when animals are immunized with whole cells as was observed in our study.

We found that NSC-6-labeled BASP1 localizes to all radial glia at the E12 stage of brain development, while postnatally, it restricts to the neurogenic areas of the mouse brain but not the cortex. This expression pattern contrasts previous study using DAB-based immunolabeling for NAP-22 (BASP1 alias) in the adult rat brain, which demonstrated robust labeling of cerebral cortex²⁷. While we do not know the basis of this difference in immunolabeling of cortex, possibilities include species variations between rat and mouse expression of BASP1, or differences in epitope recognition between the two antibodies used that could yield distinct patterns of immunoreactivity. Indeed, the two commercial BASP1 polyclonal antibodies did not immunolabel NSCs and in general, exhibited poor staining of the mouse brain tissue.

Summary: Boosting the expression of the ABCC1 gene may not only reduce amyloid plaques in the brain, it might also delay the onset of Alzheimer’s disease.

Source: TGen.

Findings of a study by the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, suggest that increasing expression of a gene known as ABCC1 could not only reduce the deposition of a hard plaque in the brain that leads to Alzheimer’s disease, but might also prevent or delay this memory-robbing disease from developing.