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Amyotrophic Lateral Sclerosis (ALS) and frontotemporal dementia (FTD) are devastating diseases in which a protein called TDP-43 ends up in the wrong part of the cell, disrupting its normal role in managing RNA.

Amyotrophic Lateral Sclerosis (ALS) can result from many different mutations in the same gene, making mutation-specific treatments challenging.

Contribution of stress-associated neurovascular alterations in Parkinson’s disease and high rates of depression

Personalized Modeling and Optimization of Transcranial Temporal Interference Stimulation in Major Depressive Disorder

Investigating the role of EPG5 in Parkinson’s Disease pathogenesis

Impairments in social cognition (SC), such as difficulties in understanding emotions, social cues, and maintaining meaningful interactions, are key contributors to the loss of social inclusion and quality of life in individuals with neurodegenerative diseases (ND).

Amyotrophic Lateral Sclerosis (ALS) is a fatal disease that progressively destroys motor neurons, leading to paralysis and death, with no current cure.

Jenna Hanrahan, a Doctoral Student at Memorial University of Newfoundland, aims to characterize the brain of a humanized mouse model of Huntington’s disease.

The Role of Brain Endocannabinoid Metabolism in Social Anxiety Disorder and Social Stress

Amyotrophic Lateral Sclerosis (ALS) is a progressive disease that destroys the motor neurons needed for movement, speech, and breathing, but new research shows that other spinal cord cells called interneurons may be affected even earlier.