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| First Name: | Glyn | | Last Name: | Wainwright | | Title: | Mr | | Advanced Degrees: | MSc CITP CEng | Country/Territory: | United Kingdom | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 18 May 2011]
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View all comments by Glyn Wainwright
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Neurodevelopmental Disorders (Down syndrome, etc.), Neuromuscular Disorders (ALS, etc.), Tauopathies, Alzheimer Disease, Parkinson Disease
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Chemistry/Pharmacology, Tau/Cytoskeleton, Oxidative Stress, Neurobiology, Neurotransmission, Protein structure/chemistry, Signal transduction, Neuroimmunology, Molecular and Cell biology, Neuropathology
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Reading and Reviewing Biochemistry in relation to advanced glycation end-products (AGE) and cholesterol |
"Nutrition and Alzheimer's disease: the detrimental role of a high carbohydrate diet"
Seneff S., Wainwright G., and Mascitelli L.
European Journal of Internal Medicine 2011
DOI:10.1016/j.ejim.2010.12.017
“Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?”
Seneff S,. Wainwright G., and Mascitelli L.
Arch Med Sci 2011; 7, 1: 8-20
DOI: 10.5114/aoms.2011.20598
“Cholesterol Lowering Therapies and Membrane Cholesterol”
Wainwright G., Mascitelli L. and Goldstein M. R. Arch Med Sci 2009; 5, 3: 289-295 |
Lifestyle (particularly dietary) changes which track the epidemiology. Subject to exploration of confounders. |
Cholesterol depletion caused by glycation of ApoE receptors - stressed neurons and protective role of beta-amyloid under conditions of depleted cholesterol. Membrane leakages, myelin depletion and deformations associated with cholesterol depletions.
A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins
concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial
infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause. |
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