Molecular pathway shared by two neurodegenerative disorders found
Scientists have gained deeper knowledge about the mislocalisation of a protein, providing a possible therapeutic target that could have implications in treating dementia.
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Scientists have gained deeper knowledge about the mislocalisation of a protein, providing a possible therapeutic target that could have implications in treating dementia.
A study has shown how Parkinson’s disease may be driven by cell stress-related biochemical events that disrupt a key cellular clean-up system.
Research from the University of Copenhagen reveals how Deep Brain Stimulation treatment of walking problems in Parkinson’s disease could be optimised by targeting specific neurons in the brainstem.
In a scientific first, researchers have discovered fundamental mechanisms by which the hippocampus region of the brain organises memories into sequences and how this can be used to plan future behaviour.
Representing a breakthrough in better understanding how tau proteins cause neurodegenerative disease, scientists have mapped the tau interactome.
The study reveals the biological mechanism that causes nerve destruction in amyotrophic lateral sclerosis (ALS), potentially leading to treatments that reverse the disease.
The study uncovered disordered signalling in the brain's cerebellum, offering a novel therapeutic target for Prader Willi syndrome.
Scientists reveal that higher levels of inflammatory chemicals involved in fat metabolism occur in people with amyotrophic lateral sclerosis.
Researchers used advanced microscopy and proteomics to unveil new findings on Huntington's disease and open avenues to future treatments.
Groundbreaking study succeeded in the intranasal delivery of an anti-depressant peptide-based drug to the brain in mouse models.
The team will receive $2 million over five years to investigate the CA2 brain region for the development of neurological therapies.
In a pre-clinical study, fibrinogen increased the death of mouse brain neurons, suggeting fibrin can have similar toxic effects on neurons.
ATH434 reversed some of the gastrointestinal damage to the enteric nervous system associated with Parkinson's disease in a pre-clinical study.
The gene therapy restored the ability of neurons to convert levodopa to dopamine and may help develop therapies to slow disease progression.
The small molecule successfully targeted the C9orf72 gene that causes amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).