Growth factor treatment to overcome Alzheimer's dysfunctional signaling.
The number of people suffering from Alzheimer's disease (AD) will increase as the world population ages, creating a huge socio-economic burden. The three pathophysiological hallmarks of AD are the cholinergic system dysfunction, the β-amyloid peptide deposition and the Tau protein hyperphosphorylation. Current treatments have only transient effects and each tends to concentrate on a single pathophysiological aspect of AD. This review first provides an overall view of AD in terms of its pathophysiological symptoms and signaling dysfunction. We then examine the therapeutic potential of growth factors (GFs) by showing how they can overcome the dysfunctional cell signaling that occurs in AD. Finally, we discuss new alternatives to GFs that help overcome the problem of brain uptake, such as small peptides, with evidence from some of our unpublished data on human neuronal cell line.
Cell-Biomaterial Biohybrid Systems, Department of Chemical and Biotechnological Engineering, Université de Sherbrooke, 2500 boul. de l'Université, Sherbrooke, Québec J1K 2R1, Canada.
Marc-Antoine
MA
Lauzon
Cell-Biomaterial Biohybrid Systems, Department of Chemical and Biotechnological Engineering, Université de Sherbrooke, 2500 boul. de l'Université, Sherbrooke, Québec J1K 2R1, Canada.
Alex
A
Daviau
Department of Chemical and Biotechnological Engineering, Université de Sherbrooke, 2500 boul. de l'Université, Sherbrooke, Québec J1K 2R1, Canada.
Bernard
B
Marcos
Cell-Biomaterial Biohybrid Systems, Department of Chemical and Biotechnological Engineering, Université de Sherbrooke, 2500 boul. de l'Université, Sherbrooke, Québec J1K 2R1, Canada. Electronic address: Nathalie.Faucheux@usherbrooke.ca.
Nathalie
N
Faucheux
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D019485:Bone Morphogenetic Proteins / Q000627:therapeutic use; D016222:Fibroblast Growth Factor 2 / Q000627:therapeutic use; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000627:therapeutic use; D007335:Insulin-Like Growth Factor II / Q000627:therapeutic use; D036341:Intercellular Signaling Peptides and Proteins / Q000627:therapeutic use*; D020932:Nerve Growth Factor / Q000627:therapeutic use; D015398:Signal Transduction; D053773:Transforming Growth Factor beta1 / Q000627:therapeutic use
D016229:Amyloid beta-Peptides; D019485:Bone Morphogenetic Proteins; D036341:Intercellular Signaling Peptides and Proteins; D053773:Transforming Growth Factor beta1; D016222:Fibroblast Growth Factor 2; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D020932:Nerve Growth Factor
Beta amyloid peptide; Bone morphogenetic proteins; Central nervous system; Cholinergic system; Tau