Friday, May 18, 2012

For Alzheimer's - something to DO, NOW...


There are a number of supplements with activity directly against the pathology in the Alzheimer’s brain. Here is just one, along with the published evidence (see references below).
Acetyl-L-Carnitine (ALCAR) is a nutritional supplement long known to have beneficial effects on the brain. In fact, more recent studies in animal models of AD showing that ALCAR inhibits several key pathways in the development of AD, including oxidative damage, the production of beta-amyloid protein, the cleavage of tau protein, apoptosis (cell self-destruction), and cellular stress intolerance.1-8
In addition, no fewer than seven double-blind placebo-controlled human trials of ALCAR in AD patients, using from 1.2 to 3 grams daily, have shown that this supplement may slow the decline in or improve performance on cognitive function tests.9-15
If anyone’s interested in a potential real solution to AD now, we’ve assembled approximately thirty elements backed by similar data that can be done now to slow progress, possibly arrest and potentially even reverse AD. We assembled them into a 6-step program in our upcoming book: Alzheimer’s, Memory Loss, MCI: The Latest Science for Prevention and Treatment. We hope to have it on Amazon by the 2nd week of June.

1.         H. M. Abdul et al., Acetyl-L-Carnitine-Induced Up-Regulation of Heat Shock Proteins Protects Cortical Neurons against Amyloid-Beta Peptide 1-42-Mediated Oxidative Stress and Neurotoxicity: Implications for Alzheimer’s Disease,” Journal of Neuroscience Research 84, no. 2 (2006): 398–408.
2.         G. Traina et al., “In the Rat Brain Acetyl-L-Carnitine Treatment Modulates the Expression of Genes Involved in Neuronal Ceroid Lipofuscinosis,” Molecular Neurobiology 38, no. 2 (2008): 146–52.
3.         G. Traina, G. Federighi, and M. Brunelli, “Up-Regulation of Kinesin Light-Chain 1 Gene Expression by Acetyl-L-Carnitine: Therapeutic Possibility in Alzheimer’s Disease,” Neurochemistry International 53, no. 6–8 (2008): 244–7.
4.         R. Epis et al., “Modulatory Effect of Acetyl-L-Carnitine on Amyloid Precursor Protein Metabolism in Hippocampal Neurons,” European Journal of Pharmacology 597, no. 1–3 (2008): 51–6.
5.         J. Suchy, A. Chan, and T. B. Shea, “Dietary Supplementation with a Combination of Alpha-Lipoic Acid, Acetyl-L-Carnitine, Glycerophosphocoline, Docosahexaenoic Acid, and Phosphatidylserine Reduces Oxidative Damage to Murine Brain and Improves Cognitive Performance,” Nutrition Research 29, no. 1 (2009): 70–4.
6.         G. Traina et al., “Cytoprotective Effect of Acetyl-L-Carnitine Evidenced by Analysis of Gene Expression in the Rat Brain,” Molecular Neurobiology 39, no. 2 (2009): 101–6.
7.         J. C. Shenk et al., “The Effect of Acetyl-L-Carnitine and R-Alpha-Lipoic Acid Treatment in ApoE4 Mouse as a Model of Human Alzheimer’s Disease,” Journal of the Neurological Sciences 283, no. 1–2 (2009): 199–206.
8.         Y. Y. Yin et al., “Acetyl-L-Carnitine Attenuates Okadaic Acid Induced Tau Hyperphosphorylation and Spatial Memory Impairment in Rats,” Journal of Alzheimer’s Disease 19, no. 2 (2010): 735–46.
9.         L. J. Thal et al., “A 1-Year Multicenter Placebo-Controlled Study of Acetyl-L-Carnitine in Patients with Alzheimer’s Disease,” Neurology 47, no. 3 (1996): 705–11.
10.       J. O. Brooks et al., “Acetyl L-Carnitine Slows Decline in Younger Patients with Alzheimer’s Disease: A Reanalysis of a Double-Blind, Placebo-Controlled Study Using the Trilinear Approach,” International Psychogeriatrics 10, no. 2 (1998): 193–203.
11.       G. Salvioli and M. Neri. “L-Acetylcarnitine Treatment of Mental Decline in the Elderly,” Drugs Under Experimental and Clinical Research 20, no. 4 (1994): 169–76.
12.       M. Sano et al., “Double-Blind Parallel Design Pilot Study of Acetyl Levocarnitine in Patients with Alzheimer’s Disease,” Archives of Neurology 49, no. 11 (1992): 1137–41.
13.       A. Spagnoli et al., “Long-Term Acetyl-L-Carnitine Treatment in Alzheimer’s Disease,” Neurology 41, no. 11 (1991): 1726–32.
14.       C. Cipolli and G. Chiari, [“Effects of L-Acetylcarnitine on Mental Deterioration in the Aged: Initial Results,”]. La Clinica Terapeutica 132, no. 6 Suppl. (1990): 479–510. [in Italian].
15.       W. M. Herrmann, B. Dietrich, and R. Hiersemenzel. “Pharmaco-Electroencephalographic and Clinical Effects of the Cholinergic Substance—Acetyl-L-Carnitine—in Patients with Organic Brain Syndrome,” International Journal of Clinical Pharmacology Research 10, 1–2 (1990): 81–4.

Thursday, May 17, 2012

Beyond Palliation. Something to do NOW.


There are a number of supplements with activity directly against the pathology in the Alzheimer’s brain. Here is just one, along with the published evidence (see references below).
Acetyl-L-Carnitine (ALCAR) is a nutritional supplement long known to have beneficial effects on the brain. In fact, more recent studies in animal models of AD showing that ALCAR inhibits several key pathways in the development of AD, including oxidative damage, the production of beta-amyloid protein, the cleavage of tau protein, apoptosis (cell self-destruction), and cellular stress intolerance.1-5
In addition, no fewer than seven double-blind placebo-controlled human trials of ALCAR in AD patients, using from 1.2 to 3 grams daily, have shown that this supplement may slow the decline in or improve performance on cognitive function tests.6-13
If anyone’s interested in a potential real solution to AD now, we’ve assembled approximately thirty elements backed by similar data that can be done now to slow progress, possibly arrest and potentially even reverse AD. We assembled them into a 6-step program in our upcoming book: Alzheimer’s, Memory Loss, MCI: The Latest Science for Prevention and Treatment. We hope to have it on Amazon by the 2nd week of June.

1.         H. M. Abdul et al., Acetyl-L-Carnitine-Induced Up-Regulation of Heat Shock Proteins Protects Cortical Neurons against Amyloid-Beta Peptide 1-42-Mediated Oxidative Stress and Neurotoxicity: Implications for Alzheimer’s Disease,” Journal of Neuroscience Research 84, no. 2 (2006): 398–408.
2.         G. Traina et al., “In the Rat Brain Acetyl-L-Carnitine Treatment Modulates the Expression of Genes Involved in Neuronal Ceroid Lipofuscinosis,” Molecular Neurobiology 38, no. 2 (2008): 146–52.
3.         G. Traina, G. Federighi, and M. Brunelli, “Up-Regulation of Kinesin Light-Chain 1 Gene Expression by Acetyl-L-Carnitine: Therapeutic Possibility in Alzheimer’s Disease,” Neurochemistry International 53, no. 6–8 (2008): 244–7.
4.         R. Epis et al., “Modulatory Effect of Acetyl-L-Carnitine on Amyloid Precursor Protein Metabolism in Hippocampal Neurons,” European Journal of Pharmacology 597, no. 1–3 (2008): 51–6.
5.         J. Suchy, A. Chan, and T. B. Shea, “Dietary Supplementation with a Combination of Alpha-Lipoic Acid, Acetyl-L-Carnitine, Glycerophosphocoline, Docosahexaenoic Acid, and Phosphatidylserine Reduces Oxidative Damage to Murine Brain and Improves Cognitive Performance,” Nutrition Research 29, no. 1 (2009): 70–4.

6.         Y. Y. Yin et al., “Acetyl-L-Carnitine Attenuates Okadaic Acid Induced Tau Hyperphosphorylation and Spatial Memory Impairment in Rats,” Journal of Alzheimer’s Disease 19, no. 2 (2010): 735–46.
7.         L. J. Thal et al., “A 1-Year Multicenter Placebo-Controlled Study of Acetyl-L-Carnitine in Patients with Alzheimer’s Disease,” Neurology 47, no. 3 (1996): 705–11.
8.         J. O. Brooks et al., “Acetyl L-Carnitine Slows Decline in Younger Patients with Alzheimer’s Disease: A Reanalysis of a Double-Blind, Placebo-Controlled Study Using the Trilinear Approach,” International Psychogeriatrics 10, no. 2 (1998): 193–203.
9.         G. Salvioli and M. Neri. “L-Acetylcarnitine Treatment of Mental Decline in the Elderly,” Drugs Under Experimental and Clinical Research 20, no. 4 (1994): 169–76.
10.       M. Sano et al., “Double-Blind Parallel Design Pilot Study of Acetyl Levocarnitine in Patients with Alzheimer’s Disease,” Archives of Neurology 49, no. 11 (1992): 1137–41.
11.       A. Spagnoli et al., “Long-Term Acetyl-L-Carnitine Treatment in Alzheimer’s Disease,” Neurology 41, no. 11 (1991): 1726–32.