Topic: Amyotrophic lateral sclerosis

Join Filippo Prischi’s group at the Randall Centre for Cell and Molecular Biophysics for a 36-month appointment. Investigate protein–RNA interactions and regulation relevant to amyotrophic lateral sclerosis, including the interaction network of Annexin A11. The work combines biological NMR, SAXS, recombinant protein preparation and cellular approaches. The role is full time, with a start no earlier than 1 November 2026. Applications close on 16 October; the employer may close recruitment earlier if application volume warrants it.

A hallmark pathological feature of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the depletion of RNA-binding protein TDP-43 from the nucleus of neurons in the brain and spinal cord. A major function of TDP-43 is as a repressor of cryptic exon inclusion during RNA splicing. By re-analyzing RNA-sequencing datasets from human FTD/ALS brains, we discovered dozens of novel cryptic splicing events in important neuronal genes. Single nucleotide polymorphisms in UNC13A are among the strongest hits associated with FTD and ALS in human genome-wi

Due to high homology to the human genome and rapid development, zebrafish have been successfully used to model diseases of the neuromuscular system. In this seminar, I will present current advances in modeling genetic causes of Amyotrophic Lateral Sclerosis (ALS), the most common motor neuron degeneration and show how epistatic interaction studies in zebrafish have helped elucidate synergistic effects of major ALS genes and their cellular targets.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, defined by motor neuron loss, muscle paralysis, and death. ALS individuals often present alterations in cardiovascular function that may evolve into heart failure and death. Mitochondrial dysfunction and oxidative stress are key players in ALS pathophysiology. Thus, improving mitochondrial function and/or antioxidant capacity constitute promising therapeutic strategies to delay ALS progression. We hypothesized that mitochondria-targeted antioxidant AntiOxCIN4 can reduce cardiac oxidative/nitrosative stress in SOD1G93A ALS mice