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A significant reduction of GABA and monoamine oxidase B (MOAB), the latter of which is an astrocytic enzyme that produces GABA, was also observed in Crym KO mice. These observations suggest that increased synaptic excitation from IOFC terminals leads to lower levels of tonic GABA, which causes reduced presynaptic inhibition.

Study significance

Crym-expressing astrocytes in the central striatum regulate the release of GABA from the IOFC into the central striatum. Importantly, the loss of this regulation can lead to perseveration, which involves the continuation or repetition of a response or activity, a phenotype that is often reported in OCD, autism, Tourette’s syndrome, and HD.

A simple blood test picking up on biomarkers of Alzheimer’s disease could help experts diagnose this condition sooner and less invasively. However, the test has not yet been brought to market.

Researchers at the University of Colorado Anschutz Medical Campus have found that inhibiting a key protein can stop the destruction of synapses and dendritic spines commonly seen in Alzheimer’s disease.

The study, whose first author is Tyler Martinez, a student in the Pharmacology and Molecular Medicine PhD program at the University of Colorado School of Medicine, was published recently in the journal eNeuro.

The researchers, using rodent neurons, found that targeting a protein called Mdm2 with an experimental cancer drug known as nutlin, stopped neurotoxic amyloid-b peptides that accumulate in Alzheimer’s disease (AD) from overly pruning synapses.

According to a Mayo Clinic study published in Nature Neuroscience, the cells that act as the central nervous system’s first line of defense against harm also play a role in helping the brain awaken from anesthesia. This discovery could help pave the way for innovative methods that address post-anesthesia complications.

When coming out of anesthesia, more than one-third of patients can experience either extreme drowsiness or hyperactivity, a side effect called delirium. Mayo researchers found that special immune cells in the brain called microglia can act to shield neurons from the aftereffects of anesthesia to awaken the brain.

“This is the first time we’ve seen microglia enhance and boost neuronal activity by physically engaging the brain circuits,” says Mayo Clinic neuroscientist Long-Jun Wu, senior author of the study.

New research has identified iron deficiencies in the blood as a major culprit in long COVID cases.

A new report from the University of Cambridge was able to connect that low iron levels contributed to inflammation and anemia and halted healthy red blood cell production in patients just two weeks after being diagnosed with COVID-19.

Many of those individuals reported having long COVID — which has recently been associated with a frightening IQ loss from brain fog — within months, according to the study, published in Nature Immunology.