Acetyl-L-Carnitine (Alcar) Provides Long-Term Neuroprotection After Traumatic Brain Injury in Immature Rats

But what about mature rats and then humans?
http://journals.lww.com/ccmjournal/Abstract/2012/12001/189___Acetyl_L_Carnitine__Alcar__Provides.156.aspx

Abstract

Introduction: Traumatic brain injury (TBI) is the leading cause of morbidity in children and survivors suffer from long-term cognitive and memory impairment. TBI is characterized by reduced aerobic cerebral energy metabolism early after injury. Exogenous acetyl-L-carnitine (ALCAR) is metabolized in the brain to acetyl coenzyme A and then enters the tricarboxylic acicoenzyme Ad cycle. ALCAR is neuroprotective in animal models of cerebral ischemia and spinal cord injury, with limited studies in TBI.

Hypothesis: Treatment with ALCAR during the first 24 h following TBI in immature rats improves neurologic outcome.

Methods: Postnatal day 21-22 rats underwent baseline MRI/MRS imaging, then were randomly assigned to sham surgery or controlled cortical impact (CCI) to the left parietal cortex. At 1, 4, 12 and 23h after injury, rats received ALCAR (100 mg/kg, intraperitoneally) or drug vehicle (normal saline). Longitudinal in vivo T2 MRI and MRS imaging was performed at 2-4hr, 24hr, 72hr, 7days and 21 days after brain trauma to assess structural and biochemical integrity. Functional recovery was assessed by battery of behavioral tests (beam walking, novel object recognition, novel object location and Morris-Water-Maze) up to 28d after TBI.

Results: TBI resulted in reduced time spent with a novel object in vehicle-treated rats compared to shams at all time points assessed (7days: 43.67 +/- 6.1% vs. 65.9 +/- 3.6%; 14days: 51.9 +/- 2.6% vs. 66.12 +/- 3.77%; 21days: 41.9 +/- 4.2% vs. 65.4 +/- 5.29%; n=11). TBI rats treated with ALCAR had improved time spent with a novel object compared to vehicle-treated injured rats (7days: 57.97 +/- 7.6%; 14days: 62.6 +/- 2.98%; 21days: 61.7 +/- 5.8%; n = 11; p < 0.05 vs. vehicle). ALCAR treated rats demonstrated improved latency to find the hidden platform in Morris water maze. Hippocampal MRS experiments revealed that ALCAR-treated immature rats had increased GABA and glutamine in the first 24hr after TBI vs. vehicle-treated injured rats.

Conclusions: Treatment with ALCAR during the first 24 h after TBI supported brain astrocytic and GABAergic neuronal metabolism acutely and improved long-term (up to 28days) neurologic outcome. Support: K08 NS 069815