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Memory Deficits in Cancer Patients With Serum NMDA Receptor Autoantibodies

Serum NMDAR autoantibodies are associated with isolated memory deficits in patients with cancer and might serve as a potential biomarker for cancer-related cognitive impairment.


ObjectivesNeuronal autoantibodies are linked to cognitive impairment in neurologic diseases and can be associated with tumors. In patients with cancer, IgA/IgM N-Methyl-D-Aspartate receptor (NMDAR) autoantibodies are most common, yet their clinical relevance is unclear. We assessed cognitive function in cancer patients with serum NMDAR autoantibodies and compared the results with matched controls.

Stem cells and adult neurogenesis

The brain has a remarkable ability to learn how to discriminate different stimuli. This video shows the work that is done within the LabEx Revive framework (www.revive.fr) in the laboratory directed by Prof. Pierre-Marie Lledo. Using mice and stem cells as a model, they have shown how adult neurogenesis is decreased or stimulated depending on different factors.

Learn more about this crucial area of stem cell research at: www.revive.fr, https://research.pasteur.fr/en/member… more about stem cells in general at www.eurostemcell.org.

Credits:
This video was made possible by the LabEx Revive (www.revive.fr), which is a selected project of the ANR \.

Johns Hopkins Scientists Identify Key Brain Protein That May Slow Alzheimer’s

Researchers at Johns Hopkins Medicine report that findings from a new study funded by the National Institutes of Health are helping to identify a promising new biological target for Alzheimer’s disease. The focus is a protein that produces a crucial gas within the brain.

Studies in genetically engineered mice show that the protein Cystathionine γ-lyase, also known as CSE, plays an essential role in forming memories, says Bindu Paul, M.S., Ph.D., an associate professor of pharmacology, psychiatry and neuroscience at the Johns Hopkins University School of Medicine who led the research. CSE is best known for generating hydrogen sulfide, the gas responsible for the smell of rotten eggs, but the new findings highlight its importance in brain function.

Mapping gene disruptions in sporadic early onset Alzheimer’s disease across key brain regions

A new study led by researchers at UTHealth Houston investigated both gene expression and regulation at single cell levels to reveal disruptions in gene function in three brain regions of patients with sporadic early onset Alzheimer’s disease.

The findings are published in Science Advances.

Only about 5% to 10% of patients with Alzheimer’s disease are younger than 65. Of those patients, 10% have mutations in the APP, PSEN1, and PSEN2 genes, which are associated with Alzheimer’s disease. The other 90% of these cases are classified as sporadic early onset Alzheimer’s, a rare and aggressive form of the disease that begins before age 65. The genetic tie in early onset Alzheimer’s is largely unidentified, representing a significant but understudied population.

One way brain ‘conductors’ find precise connection to target cells

New research reveals how a class of neurons that help coordinate communication in the brain link up with their target cells, identifying two molecules that must be present before synapses, the structures that carry signals between these partners, can form on the target neurons.

These cells are inhibitory interneurons that connect to a specific location on target excitatory neurons, regulating information processing and maintaining proper balance in brain circuits by controlling how active the excitatory neurons become. Loss of coordination between these two types of cells, which leads to circuit malfunction, is associated with such disorders as epilepsy, depression, autism and schizophrenia.

Scientists Discover Method To Erase Toxic Tau From Human Neurons

Researchers at the University of New Mexico have uncovered an unexpected role for OTULIN, an enzyme best known for its involvement in immune system regulation. The team found that OTULIN also plays a key role in the production of tau, a protein linked to many neurodegenerative disorders, along with brain inflammation and the biological processes associated with aging.

The findings were reported in the journal Genomic Psychiatry. In the study, scientists showed that disabling OTULIN stopped tau from being produced and cleared existing tau from neurons. This was achieved in two ways: by using a specially designed small molecule or by removing the gene responsible for producing the enzyme. The experiments were carried out in two types of cells, including cells derived from a person who had died from late-onset sporadic Alzheimer’s disease and human neuroblastoma cells that are commonly used in laboratory research.

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