Growing evidence exists on regulation of the chloride importer solute carrier family 12 member 2 (SLC12A2), also known as NKCC1, as a therapeutic approach to treat neurological disorders. Altered expression of NKCC1 leads to impaired intracellular chloride levels in neurons and imbalance in the excitatory-inhibitory axis in the brain.
Neuronos Ltd., a subsidiary of Beyond Air Inc.’s, has secured an initial $2 million in equity financing from private investors as part of a larger funding round. This investment will accelerate the preclinical development of Neuronos’s small-molecule drug for autism that leverages the regulation of nitric oxide (NO) levels in the brain. The company’s small-molecule therapy is based on research from Hebrew University.
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and a leading monogenic cause of autism, yet effective treatments remain elusive. Previous work showed that N-methyl-D-aspartate receptors (NMDARs) play a prominent pathophysiological role in FXS and other neurodevelopmental disorders.
Recent transcriptomic studies indicated a connection between neuroinflammation, changes in neuroimmune responses, and the development of autism spectrum disorder (ASD). The microglial calcium-binding protein A9 (S100A9) showed increased circulating levels in young adults, positively correlating with autistic severity.
T-cell leukemia homeobox protein 3 (TLX3) is a key regulator of fate specification of excitatory neurons and found expressed in proliferating granule neuron progenitors (GNPs) of the cerebellum, but its main role is not well known.
Investigators at the Institute for Research in Biomedicine (IRB Barcelona) have unraveled how and why the absence of a neuronal microexon in cytoplasmic polyadenylation element-binding 4 (CPEB4) gives rise to autism. In 2018, investigators from IRB, co-led by Raúl Méndez, identified the overt correlation between defects in CPEB4 and the onset of autism. However, the previous work did not provide the molecular mechanism explaining the correlation.
Investigators at the Institute for Research in Biomedicine (IRB Barcelona) have unraveled how and why the absence of a neuronal microexon in cytoplasmic polyadenylation element-binding 4 (CPEB4) gives rise to autism. In 2018, investigators from IRB, co-led by Raúl Méndez, identified the overt correlation between defects in CPEB4 and the onset of autism. However, the previous work did not provide the molecular mechanism explaining the correlation.
Our immune cells are not just “defenders” against deadly viruses and pathogens but also a great balancer for tissue homeostasis. For neurological disorders, understanding the neuro-immune axis could be key to treating previously untreatable conditions such as autism spectrum disorder, according to Jun R. Huh, professor of immunology at Harvard Medical School.
Our immune cells are not just “defenders” against deadly viruses and pathogens but also a great balancer for tissue homeostasis. For neurological disorders, understanding the neuro-immune axis could be key to treating previously untreatable conditions such as autism spectrum disorder, according to Jun R. Huh, professor of immunology at Harvard Medical School.
