Melanoma is the most aggressive form of skin cancer and often spreads to the brain. Though immunotherapy has greatly improved the outlook for even metastatic melanoma patients, once melanoma brain metastases (MBM) develop, prognosis worsens, and available therapeutic options decline. Scientists at the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and the Miguel Hernández University of Elche (UMH) have found a way to tackle MBM through microglial reprogramming.

The way the brain ages is not the same in women and men. A study in mice has observed differences in the expression of the maternal and paternal X chromosomes that could explain variation in brain aging between the sexes and a faster deterioration in some women. Another study has discovered different survival strategies in the microglial cells of females and males. Both studies highlight sex differences that could have implications for several age-related neurological disorders, such as Alzheimer’s or Parkinson’s.

Reducing microglial activity in the presence of apolipoprotein E4 (APOE4) has uncovered a mechanism associated with the deposition of misfolded amyloid and tau in a novel mouse model of Alzheimer’s disease. By transplanting human neurons into the mouse brain and eliminating the mouse microglia, scientists at the Gladstone Institutes in San Francisco observed that amyloid and tau deposition was reduced. These results support therapeutic strategies that target APOE4 and microglia.

Using microglia and an unbiased screening method, investigators have identified almost 60 previously unknown targets for γ-secretase. Investigators from KU Leuven and colleagues published their results in Molecular Cell on Nov. 16, 2023.

The broadest view of post-mortem brains in Alzheimer’s disease (AD) has unveiled the genome, transcriptome and epigenome alterations of this neurodegenerative condition. The coordinated research, directed by scientists at the Massachusetts Institute of Technology (MIT), also described new cellular pathways that could help the scientific community design new therapies. Four simultaneous studies published on Sept. 28, 2023, in Cell, presented a brain single-cell atlas of AD, exposed the damage that affects DNA, and described the processes that alter the microglia and dysregulate the epigenome.

The broadest view of post-mortem brains in Alzheimer’s disease (AD) has unveiled the genome, transcriptome and epigenome alterations of this neurodegenerative condition. The coordinated research, directed by scientists at the Massachusetts Institute of Technology (MIT), also described new cellular pathways that could help the scientific community design new therapies. Four simultaneous studies published on Sept. 28, 2023, in Cell, presented a brain single-cell atlas of AD, exposed the damage that affects DNA, and described the processes that alter the microglia and dysregulate the epigenome.

Alzheimer’s disease (AD) has a new candidate for its treatment. Nasal anti-CD3 monoclonal antibody (MAb) reduced microglia activation in the brain of mice without its effect being dependent on the β-amyloid (Aβ) deposits characteristic of this neurodegenerative disorder. “We have done many basic studies in the laboratory on microglia. Microglia activation occurs in many neurologic diseases. One of them is multiple sclerosis (MS). And it also occurs in AD,” senior author Howard Weiner told BioWorld.

In brain research, be it basic or clinical, neurons have long hogged the limelight. But at the 2023 European Meeting on Glial Cells in Health and Disease, neurons take a back seat to glia – cell types that have often been described as support cells and treated as an afterthought, but that play critical roles in all aspects of brain function, including information processing.