KCNJ2 inhibition: a therapeutic target for traumatic brain injury
Using cortical organoids, researchers discovered that targeting KCNJ2 could reduce nerve cell death after TBI.
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Using cortical organoids, researchers discovered that targeting KCNJ2 could reduce nerve cell death after TBI.
Researchers have presented new findings that offer potential pathways to arrest critical steps toward the accumulation of mutant tau.
Researchers discovered that NPTX2 protein accumulated in cells containing abnormal TDP-43 in FTD and ALS patients.
Researchers found that ANG in its mutated form slows stem cell differentiation, resulting in neurodevelopmental defects in adult nerve cells.
Scientists find a way to slow the progression of Huntington’s disease by analysing DNA and find the basis of a potential treatment.
Discovery about Huntington’s disease may apply to other neurodegenerative disorders, like Alzheimer’s and frontotemporal dementia.
In the sections that follow, we dive in on the latest research describing the underlying causes of ALS and a closely related condition known as frontotemporal dementia (FTD), two forms of neurodegenerative disease that share striking similarities in their molecular pathologies.
Scientists have gained deeper knowledge about the mislocalisation of a protein, providing a possible therapeutic target that could have implications in treating dementia.
Representing a breakthrough in better understanding how tau proteins cause neurodegenerative disease, scientists have mapped the tau interactome.
GlaxoSmithKline (GSK) and the University of Oxford will collaborate to investigate diseases using technologies such as functional genomics and machine learning.
The small molecule successfully targeted the C9orf72 gene that causes amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Researchers at the University of East Finland have been using skin cells to investigate pathological hallmarks in frontotemporal dementia patients.
In this article, Dr Jim Burns discusses promising pre-clinical results of how a new platform could treat the root cause of many devastating genetic diseases including myotonic dystrophy type 1.
According to researchers, the more small tau protein variants expressed by neurons, the slower neurofibrillary tangles form.
New findings on dementia reveal that brain atrophy spreads via connected brain networks, rather than simply adjacent areas of the brain.