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Despite disease-specific triggers—such as Aβ/tau, α -synuclein, mutant huntingtin, or SOD1/TDP-43—these disorders consistently exhibit impaired bioenergetics, oxidative stress, disrupted mitochondrial dynamics and trafficking, defective quality control, and calcium dysregulation, ultimately promoting neuroinflammation and cell death

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SS-31 has shown neuroprotective effects in multiple preclinical models of these conditions, reducing mitochondrial ROS, preserving synaptic function, and improving neuronal survival