Preventive Role of L-Carnitine and Balanced Diet in Alzheimer’s Disease (original) (raw)
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The role of L-carnitine in neurodegenerative disorders
Pharmakeutiki, 2009
Population ageing and modern lifestyle seem to be two important factors contributing to neurodegenerative diseases, while the underlying cellular pathophysiological mechanisms implicate the phenomenon of oxidative stress in most studies. Antioxidants such as carnitine, which neutralize directly or indirectly the action of free radicals, are suggested as pharmacological compounds which could limit these degenerative processes. In this review, we present the laboratory and clinical data on the protective effect of L-carnitine administration in neurodegenerative diseases, such as Alzheimer disease, Parkinson disease and multiple sclerosis. In addition, the potential role of carnitine in limiting degenerative events accompanying ageing, such as the decline in hearing or vision, or in limiting geriatric psychiatric diseases, is also examined.
Carnitine, carnitine acetyltransferase, and glutathione in Alzheimer brain
Neurochemical Research, 1995
Glutathione and "total" carnitine (i.e., free camitine plus acid-soluble camitine esters) were measured in an affected (superior frontal gyrus; SFG) and unaffected (cerebellum: CBL) region of Alzheimer disease (AD) and control brains. Average glutathione content in AD SFG (n = 13) and AD CBL (n = 7) (7.9 _+ 2.1 and 11.9 _ 4.0 nmol/mg protein, respectively (mean ___ S.D.)) was similar to that in control SFG (n = 13) and CBL (n = 6) (7.7 _+ 2.0 and 11.6 +_ 2.6 nmol/mg protein, respectively). However, glutathione increased significantly with age in AD brain (p = 0.003) but not in control brain. Average total camitine in AD SFG (84 _+ 47 pmol/mg protein; n = 10) and AD CBL (108 ___ 86 pmol/mg protein; n = 7) was not significantly different from that in the corresponding regions of control brain (148 _ 97 (n = 10) and 144 _ 107 (n = 6) pmol/ mg protein, respectively). However, a significant decline of total carnitine with age in both regions was noted for AD brain, but not for control brain. Carnitine acetyltransferase activity in the AD SFG (n = 13) was not significantly different from that of control SFG (n = 13) (1.83 _+ 1.05 and 2.04 _+ 0.82 nmol/min/mg protein, respectively). However, carnitine acetyltransferase activity of AD CBL (n = 7) was significantly lower than that of control CBL (n = 6) (1.33 _+ 0.88 versus 2.26 + 0.66 nmol/mirgmg protein; p = 0.05).
Annals of the New York Academy of Sciences, 2004
L-carnitine and acetyl-L-carnitine (ALC) are both used to improve mitochondrial function. Although it has been argued that ALC is better than l-carnitine in absorption and activity, there has been no experiment to compare the two compounds at the same dose. In the present experiment, the effects of ALC and L-carnitine on the levels of free, acyl, and total L-carnitine in plasma and brain, rat ambulatory activity, and biomarkers of oxidative stress are investigated. Aged rats (23 months old) were given ALC or L-carnitine at 0.15% in drinking water for 4 weeks. L-carnitine and ALC were similar in elevating carnitine levels in plasma and brain. Both increased ambulatory activity similarly. However, ALC decreased the lipid peroxidation (malondialdehyde, MDA) in the old rat brain, while L-carnitine did not. ALC decreased the extent of oxidized nucleotides (oxo8dG/oxo8G) immunostaining in the hippocampal CA1 and cortex, while L-carnitine did not. ALC decreased nitrotyrosine immunostaining in the hippocampal CA1 and white matter, while L-carnitine did not. In conclusion, ALC and L-carnitine were similar in increasing ambulatory activity in old rats and elevating carnitine levels in blood and brain. However, ALC was effective, unlike L-carnitine, in decreasing oxidative damage, including MDA, oxo8dG/oxo8G, and nitrotyrosine, in old rat brain. These data suggest that ALC may be a better dietary supplement than L-carnitine.
Acetyl-L-Carnitine in Dementia and Other Cognitive Disorders: A Critical Update
Nutrients, 2020
Several studies explored the effects of acetyl-L-carnitine (ALC) in dementia, suggesting a role in slowing down cognitive decline. Nevertheless, in 2003 a systematic review concluded there was insufficient evidence to recommend a clinical use, although a meta-analysis in the same year showed a significant advantage for ALC for clinical scales and psychometric tests. Since then, other studies have been published; however, a critical review is still lacking. We provide an update of the studies on ALC in primary and secondary dementia, highlighting the current limitations and translational implications. Overall, the role of ALC in dementia is still under debate. The underlying mechanisms may include restoring of cell membranes and synaptic functioning, enhancing cholinergic activity, promoting mitochondrial energy metabolism, protecting against toxins, and exerting neurotrophic effects. The effects of ALC on the gut–liver–brain axis seem to identify the category of patients in which th...
Nutrition & Metabolism, 2010
Carnitine is a conditionally essential nutrient that plays a vital role in energy production and fatty acid metabolism. Vegetarians possess a greater bioavailability than meat eaters. Distinct deficiencies arise either from genetic mutation of carnitine transporters or in association with other disorders such as liver or kidney disease. Carnitine deficiency occurs in aberrations of carnitine regulation in disorders such as diabetes, sepsis, cardiomyopathy, malnutrition, cirrhosis, endocrine disorders and with aging. Nutritional supplementation of L-carnitine, the biologically active form of carnitine, is ameliorative for uremic patients, and can improve nerve conduction, neuropathic pain and immune function in diabetes patients while it is life-saving for patients suffering primary carnitine deficiency. Clinical application of carnitine holds much promise in a range of neural disorders such as Alzheimer's disease, hepatic encephalopathy and other painful neuropathies. Topical application in dry eye offers osmoprotection and modulates immune and inflammatory responses. Carnitine has been recognized as a nutritional supplement in cardiovascular disease and there is increasing evidence that carnitine supplementation may be beneficial in treating obesity, improving glucose intolerance and total energy expenditure.
The role of L-carnitine in the brain aging
Pharmakeftiki, 2009
Carnitine is an important compound of cellular metabolism and it is essential for b-oxidation of lipid acids. In neural system, although b-oxidation is not the main source of energy, carnitine is involved in the regulation of energy production and calorie intake, the latter via the hypothalamus, as well as indirectly in synaptic neurotransmission. Since the above cellular processes are modified during brain aging, we aimed to review the literature on the role of carnitine in brain aging. Particular emphasis is given on the mechanisms of antioxidative action of carnitine in brain, as well as its association with cholinergic and dopaminergic system along with other various neural membrane receptors, such as the NMDA, calcium or nerve growth factor (NGF) receptors. In addition, the connection of carnitine with mechanisms of protection against cellular stress and particularly its relation with heat shock proteins (HSP), ionic channels and sodium pump, is also reviewed.
2011
Alzheimer's disease (AD) is now the most common cause of dementia in the elderly. This study aimed to explore new markers for AD as total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α); to determine the modulatory effects of vitamin E (VE), acetyl-L-carnitine (ALC) and α-lipoic acid (LA) on the investigated parameters and to evaluate the possible mechanisms for the role of these nutraceutical in regression of AD that is induced in female rats. Our results revealed that brain acetylcholine esterase (AChE) activity and tHcy levels were significantly increased in AD model. Folic acid, vitamin B 12 levels and Na + /K + ATPase activity were markedly reduced. Plasma insulin and IGF-1 levels were noticeably decreased while plasma TNF-α and IL-1β concentrations were significantly increased, indicating that abnormal inflammatory response is associated with AD. Treatment by VE, ALC or LA restored the above me...
Neuro-nutrients as anti-alzheimer's disease agents: A critical review
Critical Reviews in Food Science and Nutrition, 2018
Alzheimer's disease (AD) is characterized by a massive neuronal death causing memory loss, cognitive impairment and behavioral alteration that ultimately lead to dementia and death. AD is a multi-factorial pathology controlled by molecular events such as oxidative stress, protein aggregation, mitochondrial dysfunction and neuro inflammation. Nowadays, there is no efficient disease-modifying treatment for AD and epidemiological studies have suggested that diet and nutrition have a significant impact on the development of this disorder. Indeed, some nutrients can protect all kind of cells, including neurons. As prevention is better than cure, life style improvement, with a special emphasis on diet, should seriously be considered as an anti-AD track and intake of nutrients promoting neuronal health is the need of the hour. Diets rich in unsaturated fatty acids, polyphenols and vitamins have been shown to protect against AD, whereas saturated fatty acids-containing diets deprived of polyphenols promote the development of the disease. Thus, Mediterranean diets, mainly composed of fruits, vegetables and omega-3 fatty acids, stand as valuable, mild and preventive anti-AD agents. This review focuses on our current knowledge in the field and how one can fight this devastating neurodegenerative disorder through the simple proper modification of our life style.
2011
Alzheimer’s disease (AD) is now the most common cause of dementia in the elderly. This study aimed to explore new markers for AD as total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNFα); to determine the modulatory effects of vitamin E (VE), acetyl-L-carnitine (ALC) and α-lipoic acid (LA) on the investigated parameters and to evaluate the possible mechanisms for the role of these nutraceutical in regression of AD that is induced in female rats. Our results revealed that brain acetylcholine esterase (AChE) activity and tHcy levels were significantly increased in AD model. Folic acid, vitamin B12 levels and Na/K ATPase activity were markedly reduced. Plasma insulin and IGF-1 levels were noticeably decreased while plasma TNFα and IL-1β concentrations were significantly increased, indicating that abnormal inflammatory response is associated with AD. Treatment by VE, ALC or LA restored the above mentioned para...