Subventions financées

Rationale: Mitochondrial dysfunction has been identified as a contributing factor for bioenergetic dysregulation and neurodegeneration in the motor cortex and spinal cord of patients with ALS.

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease leading to paralysis and death within 2-5 years from disease onset.

Mutations in the SOD1 gene, leading to the misfolding and toxic aggregation of SOD1 protein, are the second leading cause of Familial Amyotrophic Lateral Sclerosis (FALS-SOD1) and emerging literature has detected misfolded SOD1 (mSOD1) in the cerebrospinal fluid (CSF) and post-mortem tissue of Sporadic ALS (SALS) patients.

Amyotrophic lateral sclerosis (ALS) is a debilitating and terminal disease.

Current biomarkers of ALS used by clinicians to help care for ALS patients have many drawbacks that may include cost, accessibility, and invasiveness of procedures.

A G4C2 repeat expansion in C9orf72 (chromosome 9 open reading frame 72), a gene of unclear function, is the most frequent genetic cause of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (C9-ALS/FTD).

TDP-43 is an essential DNA/RNA binding protein at the epicenter of Amyotrophic Lateral Sclerosis (ALS).

Brain derived neurotrophic factor (BDNF) is well recognized for its neuroprotective functions, via activation of its high affinity receptor, tropomysin related kinase B (TrkB).

While significant efforts have been made worldwide, the development of an effective therapy to significantly slow or halt amyotrophic lateral sclerosis (ALS) progression has remained elusive.

We are testing a new digital mental health solution for physicians to better manage the treatment of depression.