One unresolved question in ALS is why the neurons most susceptible to the altered/deficient EAAT2 (and neurodegeneration) come from two different populations which do not have much in common: The lower motor neurons in the spinal cord are cholinergic and project peripherally while the upper motor neurons are glutamatergic, excitatory, reside in the cerebral neocortex and target the brain stem and spinal cord (corticobulbar and corticospinal tracts)
LCACs also perturb Ca 2+ homeostasis in the cytoplasm and have been shown to disrupt myocardial contractility and electrophysiology, thereby inducing cardiomyopathy and arrhythmias [294]
The biomarker thats used is high-sensitivity CRP (hsCRP), high levels of which increase the risk of cardiovascular disease independent of all other risk factors
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