Study summary · research use only
The Effect of Acetyl-L-Carnitine (ALCAR) on Peripheral Nerve Regeneration in Animal Models: A Systematic Review
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This systematic review and meta-analysis pooled animal studies, published from 1994 to 2018, of Acetyl-L-Carnitine (ALCAR) administered to rats with sciatic nerve injury against a control group. The authors describe ALCAR as a compound involved in mitochondrial oxidative metabolism with anti-oxidant properties. Studies were grouped by route of administration (oral in drinking water or intra-peritoneal injection), and results were combined in Revman5.4 software. The abstract reports that, across the included studies, ALCAR was associated with an increased tolerance threshold to thermal and mechanical stimuli, reduced latency, and reduced apoptosis. The authors state that the mechanisms underlying these observations remain unclear and that further studies are needed to clarify them.
Abstract
Peripheral neuropathies caused by the peripheral nervous system (PNS) damage can occur due to trauma and other disorders. They present as altered sensation, weakness, autonomic symptoms, and debilitating pain syndrome with a wide range of clinical signs. Acetyl-L-Carnitine (ALCAR) is a biological compound with essential roles in mitochondrial oxidative metabolism and anti-oxidant effects that protects mitochondria from oxidative damage and inhibits apoptosis caused by mitochondrial damage. This study is a systematic review and meta-analysis of the effects of ALCAR on peripheral nerve injuries. This review examines studies on treating traumatic peripheral neuropathies in which ALCAR is administered to rats with sciatic nerve injury with an appropriate control group. The articles were divided based on the mode of ALCAR administration. If one method was used in more than one article, their results were entered in the "Revman5.4" software and were meta-analyzed. Studies were selected from 1994 to 2018 on rats with varying physical injuries to their sciatic nerves. In one study, ALCAR was provided to rats in their drinking water, while in other studies, ALCAR was injected intra-peritoneally. Different mechanisms of ALCAR actions have been suggested in this study, but the underpinnings of the neuroprotective effects of ALCAR are still unclear. Further studies are mandatory to clarify the actual mechanisms of the neuroprotective activity of ALCAR. Based on the results of existing studies, ALCAR effectively increases the tolerance threshold of thermal and mechanical stimuli, reduces latency, and reduces apoptosis; finally, adjusting the dose and duration of administration may increase the dose and duration axon diameter.
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