Funded Grants

In late 2011, a landmark discovery was made which identified that abnormalities (mutation) in a gene called C9ORF72 were responsible for the highest percentage of hereditary ALS and frontotemporal dementia cases.

In recent years, it was discovered that a microscopic worm called C. elegans could mimic some of the aspects of human ALS when they were engineered to have abnormal (mutant) genes that cause the disease.

This project will use cells found in bone marrow as a potential means of delivering treatments to the diseased area in brain and spinal cord.

Motor neurons are made up of three distinct regions. The top of the neuron is composed of branches like a tree called dendrites that receive information to transmit.

Alzheimer’s disease (AD) is a severely disabling illness with biological causes that are not well understood. Abnormalities in gene function impacts brain activities and could cause AD.

In Alzheimer s disease (AD), critical synaptic connections between neurons disintegrate and cells die.

The existence of different strains of misshapen proteins in the brains of Alzheimer’s disease (AD) patients is emerging as an obstacle to the development of effective treatments.

Currently, AD diagnosis can only be confirmed post-mortem by observing two AD hallmarks in the brain, β-amyloid (Aβ) plaques and tau strands.

This project proposes to integrate the low-invasive, non-lethal in vivo sampling/sample preparation SPME approach with MS detection to obtain the full profile of brain metabolome and lipidome, the quantification of drugs and monitoring of their metabolism, selective extraction of target compounds (drugs or selected endogenous metabolite), as well as high resolution chemical imaging of deep brain structure.

Toxic amyloid proteins are known to be a significant contributing factor in the development of Alzheimer’s disease.