SPARC Related-Metabolic Warhead
Research and Development
Alzheimer’s disease therapeutics have historically focused on amyloid clearance, kinase inhibition, or tau immunotherapy. Yet these approaches do not directly correct the biochemical lesion most closely linked to neurodegeneration: tau hyperphosphorylation. Hyperphosphorylated tau loses its stabilizing function, misfolds, aggregates, and disseminates throughout the brain via extracellular pathways. Pathological modifications and especially their extracellular spread are central to AD progression.
In contrast to conventional approaches, emerging data show that
active catalytic reversal of tau hyperphosphorylation can meaningfully reduce pathology.
Long Shot Solutions
LMP-CT Chimera
Utilizing the Lysosomal trafficking pathways to reduce the accumulation of Amyloids.
