🎯 Drug Targets

Direct PLIN2 inhibitors would reduce lipid droplet formation and stability, promoting lipid mobilization and reducing pathological lipid accumulation. Indirect approaches target upstream regulators of PLIN2 expression or modulate associated lipases to alter lipid storage dynamics in metabolic and neurodegenerative disease states.

Drugs targeting GAP43 would enhance axonal growth cone formation and synaptic plasticity by promoting phosphorylation or membrane translocation of GAP43, thereby facilitating neurite outgrowth and synapse formation. Alternatively, agents could upregulate GAP43 expression to restore neuronal connectivity and compensate for age-related decline in neurodegenerative conditions.

Tight junction protein modulation - no established druggable mechanisms

Tight junction protein modulation - no established druggable mechanisms

Drugs targeting MAP6 would stabilize microtubules through direct binding or modulation of MAP6's stabilizing activity, thereby promoting neuronal cytoskeletal integrity and synaptic function. This stabilization could enhance axonal transport, prevent neuronal degeneration, and support cognitive and synaptic plasticity in neurodegenerative conditions.