Neurochemical abnormalities in Alzheimer’s disease and Parkinson’s disease — a comparative review

Gsell, W.; Strein, I.; Krause, U.; Riederer, Peter

doi:10.1007/978-3-7091-6846-2_12

Cited by 13 publications

(7 citation statements)

References 58 publications

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“…Thus, the effect of β-amyloid or oxidative stress can alter the internal metabolism of the endothelial cells, which may imply, among others, a corrupt production of BM constituents. Oxidative stress is considered to be a contributing factor in the development of both AD and PD [19,20,33]. In addition to inducing neuronal damage, accumulating oxygen radicals may interfere with capillary ultrastructure by expressing a toxic influence on endothelial metabolism in AD and PD.…”

Section: Discussionmentioning

confidence: 99%

Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

Farkas¹,

Jong²,

Vos³

et al. 2000

Acta Neuropathologica

190

127

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Section: Discussionmentioning

confidence: 99%

Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

Farkas¹,

Jong²,

Vos³

et al. 2000

Acta Neuropathologica

190

127

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“…Since oxidative stress is characterized by an imbalance in radical production of reactive oxygen species (ROS) and antioxidative defense, both are considered to have a major role in the process of age-related neurodegeneration and cognitive decline. [1][2][3][4][5][6][7][8][9] Evidence of oxidative stress in AD is manifested through high levels of oxidised proteins, advanced glycation end products, lipid peroxidation end products, formation of toxic species, such as peroxides, alcohols, aldehydes, free carbonyles, ketones, cholestenone and oxidative modifications in nuclear and mitochondrial DNA. [10][11][12][13][14][15][16][17][18][19][20][21] Age-related memory impairments correlate with a decrease in brain and plasma antioxidants defense mechanism.…”

Section: Oxidative Stress and Alzheimer Diseasementioning

confidence: 99%

Oxidative stress in Alzheimer disease

Gella

Durany

2009

Cell Adhesion & Migration

363

211

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Alzheimer disease (AD) is a progressive dementia affecting a large proportion of the aging population. The histopathological changes in AD include neuronal cell death, formation of amyloid plaques and neurofibrillary tangles. There is also evidence that brain tissue in patients with AD is exposed to oxidative stress (e.g., protein oxidation, lipid oxidation, DNA oxidation and glycoxidation) during the course of the disease. Advanced glycation endproducts (AGEs) are present in amyloid plaques in AD, and its extracellular accumulation may be caused by an accelerated oxidation of glycated proteins. AGEs participate in neuronal death causing direct (chemical) and indirect (cellular) free radical production and consequently increase oxidative stress. The development of drugs for the treatment of AD that breaks the vicious cycles of oxidative stress and neurodegeneration offer new opportunities. These approaches include AGE-inhibitors, antioxidants and anti-inflammatory substances, which prevent free radical production.

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“…Moreover both Fe and ascorbate, which together may enhance oxidant production and lipid peroxidation, are found in large quantities in brain tissue. This high oxidative insult is further enhanced in the presence of neurodegenerative disorders, especially AD [1][2][3][4][5] . The presence of amyloid…”

Section: Introductionmentioning

confidence: 99%

Functional Vitamin E Deficiency in <i>ApoE4</i> Patients with Alzheimer’s Disease

Mas¹,

Dupuy

Artéro

et al. 2006

Dement Geriatr Cogn Disord

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Oxidative stress has been implicated in the development of Alzheimer’s disease (AD). Consequently, antioxidant therapies including Vitamin E (VitE) supplementation for both prevention and treatment of neurodegenerative diseases currently appears to be a promising avenue of research. The aim of the present study was to examine the relationship between AD and the ApoE phenotype, lipid parameters and VitE levels in a large cohort of elderly subjects. No absolute deficit was observed in plasma VitE levels. However in AD, ApoE4 is not associated with an increase in total cholesterol (TC) and VitE levels. Moreover, our results suggest that oxidative stress-induced injury and protection by VitE in AD are related to the ApoE phenotype. Our study strongly supports the hypothesis of an impairment of lipophilic antioxidant delivery to neuronal cells in AD leading to a tissular antioxidant deficiency which could facilitate oxidative stress.

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Neurochemical abnormalities in Alzheimer’s disease and Parkinson’s disease — a comparative review

Cited by 13 publications

References 58 publications

Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

Oxidative stress in Alzheimer disease

Functional Vitamin E Deficiency in <i>ApoE4</i> Patients with Alzheimer’s Disease

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