A Thread for Glen

[HysteryDiagnosis]

http://www.ncbi.nlm.nih.gov/pubmed/12117551
Pycnogenol protects neurons from amyloid-beta peptide-induced apoptosis.
Peng QL, Buz'Zard AR, Lau BH.
Source

Department of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, Loma Linda, CA 92350, USA.
Abstract

Neuronal apoptosis is one of the pathological features of Alzheimer's disease (AD). Morphological pathology reveals that neuronal apoptosis is associated with senile plaques containing amyloid-beta peptide (Abeta) in AD brains. Reactive oxygen species (ROS) has been proposed to be involved in the apoptotic mechanism of Abeta-mediated neurotoxicity. In the present study, using a rat pheochromocytoma (PC12) cell line, we investigated the effect of Pycnogenol (PYC), a potent antioxidant and ROS scavenger, on Abeta(25-35)-induced apoptosis and ROS generation. We used vitamin E, a known antioxidant agent, to verify the effect of PYC. Abeta(25-35)-induced apoptosis in PC12 cells was demonstrated by: (1) a dose-dependent loss of cell viability; (2) a time- and dose-dependent increase in the apoptotic cells; (3) an induction of DNA fragmentation; and (4) an increase in caspase-3 activity and cleavage of poly (ADP-ribose) polymerase (PARP).

Our data showed that a significant increase in ROS formation preceded apoptotic events after PC12 cells were exposed to Abeta(25-35). We further found that PYC not only suppressed the generation of ROS but also attenuated caspase-3 activation, DNA fragmentation, PARP cleavage, and eventually protected against Abeta-induced apoptosis. Vitamin E also suppressed cell death and caspase-3 activation induced by Abeta(25-35). Taken together, these results suggest that ROS may be involved in Abeta-induced apoptosis in PC12 cells. They further suggest that PYC can reduce apoptosis, possibly by decreasing free radical generation in PC12 cells.

PMID:
12117551



Pycnogenol protects vascular endothelial cells from beta-amyloid-induced injury.
Liu F, Lau BH, Peng Q, Shah V.
Source

Department of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, CA 92350, USA.
Abstract

The neuropathological hallmarks of Alzheimer's disease (AD) are senile plaques, cerebrovascular beta-amyloidosis, neurofibrillary tangles, and selective neuronal loss. Beta-amyloid (Abeta) has been shown to cause vascular damage mediated by generation of reactive oxygen species and this damage is considered an early event in the development of AD. In this study, we determined the effect of pyenogenol, a potent antioxidant phytochemical, on Abeta-induced cellular injury. Pulmonary artery endothelial cells (PAEC) were exposed to Abeta for 24 h. Cell injury was assessed by measuring cell viability with methylthiazol tetrazolium (MTT) assay, and by determining the release of intracellular lactate dehydrogenase (LDH).

Lipid peroxidation products of PAEC were determined by measuring thiobarbituric acid-reactive substances (TBARS). Exposure of PAEC to Abeta resulted in a decrease in cell viability, an increase of LDH release indicating membrane damage, and an elevated level of TBARS. Preincubation of PAEC with pycnogenol significantly minimized these changes. This study demonstrated that pycnogenol can protect vascular endothelial cells from Abeta-induced injury. The data suggest that pycnogenol may be useful for the prevention and/or treatment of vascular or neurodegenerative diseases associated with Abeta toxicity.

PMID:
10864026

[Bluebear]

1. What a warm tribute :)

[HysteryDiagnosis]

2. Some of this stuff might delay the inevitable... and it certainly would not hurt him.

http://www.ncbi.nlm.nih.gov/pubmed/21360003

Mol Neurobiol. 2011 Mar 1.
Neuroprotection by Spice-Derived Nutraceuticals: You Are What You Eat!
Kannappan R, Gupta SC, Kim JH, Reuter S, Aggarwal BB.
Source

Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Abstract

Numerous lines of evidence indicate that chronic inflammation plays a major role in the development of various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, brain tumor, and meningitis. Why these diseases are more common among people from some countries than others is not fully understood, but lifestyle factors have been linked to the development of neurodegenerative diseases. For example, the incidence of certain neurodegenerative diseases among people living in the Asian subcontinent, where people regularly consume spices, is much lower than in countries of the western world.

Extensive research over the last 10 years has indicated that nutraceuticals derived from such spices as turmeric, red pepper, black pepper, licorice, clove, ginger, garlic, coriander, and cinnamon target inflammatory pathways, thereby may prevent neurodegenerative diseases. How these nutraceuticals modulate various pathways and how they exert neuroprotection are the focus of this review.

PMID:
21360003



http://www.ncbi.nlm.nih.gov/pubmed/21166677
J Neurochem. 2011 May;117(3):388-402. doi: 10.1111/j.1471-4159.2010.07145.x. Epub 2011 Mar 14.
Oxidative insults to neurons and synapse are prevented by aged garlic extract and S-allyl-L-cysteine treatment in the neuronal culture and APP-Tg mouse model.
Ray B, Chauhan NB, Lahiri DK.
Source

Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Abstract

Alzheimer's disease (AD) is one of the most common forms of dementia in the elderly. In AD patients, β-amyloid peptide (Aβ) plaques and neurofibrillary tangles are common features observed in the CNS. Aβ deposition results in the production of reactive oxygen species (ROS) leading to the hyperphosphorylation of tau that are associated with neuronal damage. Cholinesterase inhibitors and a partial NMDA receptor antagonist (memantine) have been identified as potential treatment options for AD. However, clinical studies have found that these drugs fail to prevent the disease progression. From ancient times, garlic (Allium sativum) has been used to treat several diseases. By 'aging' of garlic, some adverse reactions of garlic can be eliminated.

Recent findings suggest that 'aged garlic extract' (AGE) may be a therapeutic agent for AD because of its antioxidant and Aβ lowering properties. To date, the molecular properties of AGE have been sparsely studied in vitro or in vivo. The present study tested specific biochemical and molecular effects of AGE in neuronal and AD rodent models. Furthermore, we identified S-allyl-L-cysteine (SAC) as one of the most active chemicals responsible for the AGE-mediated effect(s). We observed significant neuroprotective and neurorescue properties of AGE and one of its ingredients, SAC, from ROS (H(2)O(2))-mediated insults to neuronal cells.

Treatment of AGE and SAC were found to protect neuronal cells when they were independently co-treated with ROS. Furthermore, a novel neuropreservation effect of AGE was detected in that pre-treatment with AGE alone protected ∼ 80% neuronal cells from ROS-mediated damage. AGE was also found to preserve pre-synaptic protein synaptosomal associated protein of 25 kDa (SNAP25) from ROS-mediated insult. For example, treatment with 2% AGE containing diet and SAC (20 mg/kg of diet) independently increased (∼70%) levels of SNAP25 and synaptophysin in Alzheimer's amyloid precursor protein-transgenic mice, of which the latter was significantly decreased in AD. Taken together, the neuroprotective, including preservation of pre-synaptic proteins by AGE and SAC can be utilized in future drug development in AD.

© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry.

http://www.ncbi.nlm.nih.gov/pubmed/16402761
Ann Clin Psychiatry. 2005 Oct-Dec;17(4):269-86.
A review of antioxidants and Alzheimer's disease.
Frank B, Gupta S.
Source

Department of Psychiatry, University of Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY, USA. [e-mail]
Abstract
BACKGROUND:

In this article, we review a diverse body of research and draw conclusions about the usefulness, or lack there-of, of specific antioxidants in the prevention of Alzheimer's disease (AD).
METHODS:

The National Library of Medicine's database was searched for the years 1996-2004 using the search terms "Alzheimer's, anti-oxidants, antioxidants."
RESULTS:

Over 300 articles were identified and 187 articles were selected for inclusion based on relevance to the topic. Agents that show promise in helping prevent AD include: 1) aged garlic extract, 2) curcumin, 3) melatonin, 4) resveratrol, 5) Ginkgo biloba extract, 6) green tea, 7) vitamin C and 8) vitamin E.
CONCLUSIONS:

While the clinical value of antioxidants for the prevention of AD is often ambiguous, some can be recommended based upon: 1) epidemiological evidence, 2) known benefits for prevention of other maladies, and 3) benign nature of the substance. Long-term, prospective studies are recommended.

PMID:
16402761


Publication Types, MeSH Terms, Substances

[Maccagirl]

3. Poor Glen Campbell

I wouldn't wish this hellish disease on anyone.

[Scuba]

4. Operation pyenogenol is status blue. Repeat. Operation pyenogenol is status blue.

[HysteryDiagnosis]

5. .... you missed again. n/t