Modern medicine treats Alzheimer's, ALS, and Parkinson's as distinct chemical imbalances. We see them as a singular structural failure.
A motor neuron is a supply chain stretching up to a meter long. When the "tracks" (Microtubules) break or the "engines" (Kinesin/Dynein) stall, the synapse starves.
This is the Traffic Jam Theory. The protein aggregates are not the cause; they are the pile-up resulting from a broken road.
We mapped the invariant path to cell death. It doesn't start with inflammation; it starts with transport.
We have operationalized our hypothesis into four distinct research modules covering the lifecycle of neuronal waste and energy.
Target: Aggregates (Tau, Alpha-synuclein)
We analyze the physical burden. Why do proteins misfold? How do they aggregate? We distinguish between "moveable waste" and "immovable blockages" to understand the load on the transport system.
Target: Microtubule Stability
The Core Mission. We study what holds the tubulin polymer together. We identify small molecules that act as "super-glue" to reinforce the tracks against oxidative stress and enzymatic severing.
Target: Lysosome & vATPase
Delivery is useless if the incinerator is broken. We focus on the vATPase proton pump to ensure the Lysosome maintains the acidic pH (4.5) required to degrade the cargo we deliver.
Target: ER-Mitochondria Axis
We map the "Self-Destruct" signal. How ER stress opens Ca2+ channels, triggers MAMs, and forces Mitochondria to release the ROS that burns down the highway. We aim to block this signal.
Biology is hardware. We debug it in-silico.
We do not rely on trial-and-error in wet labs. We utilize high-fidelity Computer-Aided Drug Design (CADD) pipelines to simulate the axonal environment at atomic resolution.
We filter millions of molecular structures to find the few that can penetrate the Blood-Brain Barrier and dock precisely into the Microtubule lattice or Kinesin motor complex. We simulate the cure before we synthesize it.
The goal is absolute: To find the candidates that fix the system.
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