Stem Cell Therapy and Amyotrophic Lateral Sclerosis

Stem Cell Therapy and Amyotrophic Lateral Sclerosis 

Calcium channel blockers antagonize excitatory amino acid receptor activation. A randomized, double blind, placebo controlled, crossover study of nimodipine w as conducted in 

Motor neurons may have a high threshold to activation of the heat shock protein pathw ay, w hich is involved in protein repair. Arimoclomol, an inducer of heat shock proteins, delays disease progression and improves survival in the murine model (Kieran et al., 2004). Early phase trials w ith arimoclomol in patients w ith ALS are currently underw ay. 

Statins, used predominantly in the treatment of hypercholesterolemia, act by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which regulates the synthesis of cholesterol. Statins are also agonists of peroxisome proliferator activated receptors (PPARs), which are part of the nuclear receptor superfamily and when activated, can suppress transcription of pro-inflammatory genes (Chinetti et al., 2000). In vitro and in vivo studies have shown that a decrease in serum cholesterol inhibits the production of beta amyloid and plaque (Simons et al., 1998 Fassbender et al., 

The mechanism of how lowering cholesterol affects beta amyloid production is still unclear studies have demonstrated that statins do not alter beta amyloid morphology (Hoglund et al., 2004). It may be that the neuroprotective properties of statins are due to antioxidant and anti-inflammatory effects. 

A randomized, controlled trial evaluating the efficacy of simvastatin on disease progression in patients with AD provided conflicting results. Overall, the plasma levels of beta amyloid protein remained relatively unchanged after 6 months of treatment, but those with better cognitive function demonstrated a greater reduction in beta amyloid protein levels than patients with more severe dementia (Simons et al., 

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