Acetyl-l-carnitine treatment increases nerve growth factor levels and choline acetyltransferase activity in the central nervous system of aged rats

Taglialatela, Giulio; Navarra, D.; Cruciani, Ricardo A.; Ramacci, M. T.; Alemà, G; Angelucci, L.

doi:10.1016/0531-5565(94)90062-0

Cited by 48 publications

(27 citation statements)

References 42 publications

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“…41 Taglialatela et al 42 reported that ALCAR: (1) enhances the response of PC12 cells to NGF suggesting that ALCAR may increase the response of aged neurons to neurotrophic factors within the CNS; (2) stimulates NGF receptors and neurite growth in PC12 cells; 43,44 and (3) increases NGF levels and choline acetyltransferase activity in rat CNS. 45 Piovesan et al 46 demonstrated that ALCAR increases choline acetyltransferase activity and NGF levels in the CNS of adult rats pretreated by total fimbria-fornix transection; these animals exhibit impairment of cholinergic activity similar to that seen during senescence. Taglialatela et al 47 also reported that ALCAR improves spatial memory performance in aged rats with decreased intermediate performance associated with reduction of NGF levels in the basal forebrain, suggesting a non linear relationship between spatial memory performance and basal forebrain NGF levels.…”

Section: Alcar's Modulation Of Proteins and Peptidesmentioning

confidence: 99%

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

2000

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Acetyl-L-carnitine (ALCAR) contains carnitine and acetyl moieties, both of which have neurobiological properties. Carnitine is important in the ␤-oxidation of fatty acids and the acetyl moiety can be used to maintain acetyl-CoA levels. Other reported neurobiological effects of ALCAR include modulation of: (1) brain energy and phospholipid metabolism; (2) cellular macromolecules, including neurotrophic factors and neurohormones; (3) synaptic morphology; and (4) synaptic transmission of multiple neurotransmitters. Potential molecular mechanisms of ALCAR activity include: (1) acetylation of -NH 2 and -OH functional groups in amino acids and N terminal amino acids in peptides and proteins resulting in modification of their structure, dynamics, function and turnover; and (2) acting as a molecular chaperone to larger molecules resulting in a change in the structure, molecular dynamics, and function of the larger molecule. ALCAR is reported in double-blind controlled studies to have beneficial effects in major depressive disorders and Alzheimer's disease (AD), both of which are highly prevalent in the geriatric population. Molecular Psychiatry (2000) 5, 616-632.

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Section: Alcar's Modulation Of Proteins and Peptidesmentioning

confidence: 99%

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

2000

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“…ALCAR has a large number of actions that produce acute analgesic effects (Patacchioli et al, 1989;Piovesan et al, 1995;Taglialatela et al, 1994;Ghelardini et al, 2002;Calabrese et al, 2005;Zanelli et al, 2005;Binienda et al,. 2006;Chiechio et al, 2006).…”

Section: The Analgesic Effect Of the Prophylactic Alcar Dosing Protocolmentioning

confidence: 99%

Prevention of paclitaxel-evoked painful peripheral neuropathy by acetyl-l-carnitine: Effects on axonal mitochondria, sensory nerve fiber terminal arbors, and cutaneous Langerhans cells

Jin

Flatters

Xiao

et al. 2008

Experimental Neurology

142

132

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Prophylactic treatment with acetyl-L-carnitine (ALCAR) prevents the neuropathic pain syndrome that is evoked by the chemotherapeutic agent, paclitaxel. The paclitaxel-evoked pain syndrome is associated with degeneration of the intraepidermal terminal arbors of primary afferent neurons, with the activation of cutaneous Langerhans cells, and with an increased incidence of swollen and vacuolated axonal mitochondria in A-fibers and C-fibers. Previous work suggests that ALCAR is neuroprotective in other nerve injury models and that it improves mitochondrial dysfunction. Thus, we examined whether the prophylactic efficacy of ALCAR was associated with the prevention of intraepidermal terminal arbor degeneration, the inhibition of Langerhans cell activation, or the inhibition of swelling and vacuolation of axonal mitochondria. In animals with a confirmed ALCAR effect, we found no evidence of a neuroprotective effect on the paclitaxel-evoked degeneration of sensory terminal arbors or an inhibition of the paclitaxel-evoked activation of Langerhans cells. However, ALCAR treatment completely prevented the paclitaxel-evoked increase in the incidence of swollen and vacuolated C-fiber mitochondria, while having no effect on the paclitaxel-evoked changes in A-fiber mitochondria. Our results suggest that the efficacy of prophylactic ALCAR treatment against the paclitaxel-evoked pain may be related to a protective effect on C-fiber mitochondria.

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“…Aside from its role in fatty acid -oxidation, many other functions have been attributed to L-acetylcarnitine. It has been reported that L-acetylcarnitine modulates the activity of nerve growth factor (NGF) in the nervous system in rats [1,40,52], increases the activity of choline acetyltransferase, enhances the expression of NGF receptors in the striatum and hippocampus of rats during development [10] and modulates different neurotransmitter systems including the cholinergic and dopaminergic system [24,20]. Additionally L-acetylcarnitine functions as a donor of acetyl groups in oxidative glycolysis [4] and can also have important biological function due to its ability to contribute to acetylation of -OH or -NH 2 functional groups on amino acids and Nterminal groups in proteins and peptides [39].…”

Section: Biological Properties Of L-acetylcarni-tinementioning

confidence: 99%

L-Acetylcarnitine: A Proposed Therapeutic Agent for Painful Peripheral Neuropathies

Chiechio¹,

Copani²,

Nicoletti³

et al. 2006

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During the past two decades, many pharmacological strategies have been investigated for the management of painful neuropathies. However, neuropathic pain still remains a clinical challenge. A combination of therapies is often required, but unfortunately in most cases adequate pain relief is not achieved. Recently, attention has been focused on the physiological and pharmacological effects of L-acetylcarnitine in neurological disorders. There are a number of reports indicating that L-acetylcarnitine can be considered as a therapeutic agent in neuropathic disorders including painful peripheral neuropathies. In this review article, we will examine the antinociceptive and the neuroprotective effects of Lacetylcarnitine as tested in clinical studies and in animal models of nerve injury.

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Acetyl-l-carnitine treatment increases nerve growth factor levels and choline acetyltransferase activity in the central nervous system of aged rats

Cited by 48 publications

References 42 publications

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

Prevention of paclitaxel-evoked painful peripheral neuropathy by acetyl-l-carnitine: Effects on axonal mitochondria, sensory nerve fiber terminal arbors, and cutaneous Langerhans cells

L-Acetylcarnitine: A Proposed Therapeutic Agent for Painful Peripheral Neuropathies

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