Subventions financées

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.

The team wants to take a new breakthrough technology called Cyto-iGluSnFR (pronounced “sight-oh-eye-glue-sniffer”) and adapt it for the discovery of drugs to treat a variety of brain and eye diseases.

The blood-brain barrier (BBB) plays an essential role in protecting the brain from blood-borne diseases.

No medications exist that can stop or even slow the progression for Alzheimer Disease (AD).

Two diseases that show very different trajectories have nevertheless led researchers to identify dysfunction in a common brain network.