Increased CSF F
            <sub>2</sub>
            -isoprostane concentration in probable AD

Montine, Thomas J.; Beal, M. Flint; Cudkowicz, Merit; O’Donnell, Heather; Margolin, Richard; McFarland, Lynne L.; Bachrach, A; Zackert, William E.; Roberts, L. Jackson; Morrow, Jason D.

doi:10.1212/wnl.52.3.562

Cited by 236 publications

(114 citation statements)

References 9 publications

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“…They are selectively increased in affected regions of AD brains as well as in CSF of patients with AD (Praticò et al 1998b(Praticò et al , 2000Montine et al 1999), and correlate with the amount of amyloid deposited in the Tg2576 (Praticò et al 2001b).…”

Section: Discussionmentioning

confidence: 96%

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury

Conte

Uryu

Fujimoto

et al. 2004

Journal of Neurochemistry

144

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Traumatic brain injury is a well-recognized environmental risk factor for developing Alzheimer's disease. Repetitive concussive brain injury (RCBI) exacerbates brain lipid peroxidation, accelerates amyloid (Ab) formation and deposition, as well as cognitive impairments in Tg2576 mice. This study evaluated the effects of vitamin E on these four parameters in Tg2576 mice following RCBI. Eleven-month-old mice were randomized to receive either regular chow or chow-supplemented with vitamin E for 4 weeks, and subjected to RCBI (two injuries, 24 h apart) using a modified controlled cortical impact model of closed head injury. The same dietary regimens were maintained up to 8 weeks post-injury, when the animals were killed for biochemical and immunohistochemical analyses after behavioral evaluation. Vitamin E-treated animals showed a significant increase in brain vitamin E levels and a significant decrease in brain lipid peroxidation levels. After RBCI, compared with the group on regular chow, animals receiving vitamin E did not show the increase in Ab peptides, and had a significant attenuation of learning deficits. This study suggests that the exacerbation of brain oxidative stress following RCBI plays a mechanistic role in accelerating Ab accumulation and behavioral impairments in the Tg2576 mice.

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Section: Discussionmentioning

confidence: 96%

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury

Conte

Uryu

Fujimoto

et al. 2004

Journal of Neurochemistry

144

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“…This same result was replicated in additional groups of probable AD patients and controls using both the original method [113][114][115] and the modified method [108], although the latter showed an average increase in LOAD exceeding 200%. In distinction to autopsy studies where tissue oxidative damage markers were equivalent in brains of patients with MCI and LOAD, lumbar CSF F 2 -IsoPs concentrations from MCI patients were intermediate between those from controls and patients with probable AD [116].…”

Section: Biofluid Studiesmentioning

confidence: 67%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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“…Among the isoprostanes, 8-isoprostane is considered a reliable and stable marker for free radical generation in vivo. 43,44 Additionally, 8-isoprostane is an active vasoconstrictor at physiologic concentrations and thus may be involved in vascular changes during spinal cord disease. 45 Measurement of biomarkers may be useful for the detection and prognosis of neurodegenerative diseases.…”

Section: 2mentioning

confidence: 99%

“…Degenerative myelopathy is a disease of insidious onset, which makes detection of a biochemical mediator difficult. 44 A plausible explanation for lack of differences may be that the quantities of 8-isoprostane do not reflect the actual disease process. However, in 1 dog, 8-isoprostane was measured at 2 different times with no meaningful difference between samples.…”

Section: 2mentioning

confidence: 99%

Clinical Characterization of a Familial Degenerative Myelopathy in Pembroke Welsh Corgi Dogs

et al. 2007

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Background: Adult dogs with degenerative myelopathy (DM) have progressive ataxia and paresis of the pelvic limbs, leading to paraplegia and euthanasia. Although most commonly reported in German Shepherd dogs, high disease prevalence exists in other breeds.Objective: Our aim was the clinical and histopathologic characterization of familial degenerative myelopathy (FDM) in Pembroke Welsh Corgi (PWC) dogs.Animals: Twenty-one PWCs were prospectively studied from initial diagnosis until euthanasia. Methods: Neurologic examination, blood tests, cerebrospinal fluid (CSF) analysis, electrodiagnostic testing, and spinal imaging were performed. Concentrations of 8-iso-prostaglandin F 2 a (8-isoprostane) were measured in CSF. Routine histochemistry was used for neuropathology. Deoxyribonucleic acid and pedigrees were collected from 110 dogs.Results: Median duration of clinical signs before euthanasia was 19 months. Median age at euthanasia was 13 years. All dogs were nonambulatory paraparetic or paraplegic, and 15 dogs had thoracic limb weakness at euthanasia. Electrodiagnostic testing and spinal imaging were consistent with noncompressive myelopathy. No significant difference was detected in 8-isoprostane concentrations between normal and FDM-affected dogs. Axonal and myelin degeneration of the spinal cord was most severe in the dorsal portion of the lateral funiculus. Pedigree analysis suggested a familial disease.Conclusions and Clinical Importance: Clinical progression of FDM in PWC dogs was similar to that observed in other breeds but characterized by a longer duration. Spinal cord pathology predominates as noninflammatory axonal degeneration. Oxidative stress injury associated with 8-isoprostane production is not involved in the pathogenesis of FDM-affected PWC dogs. A familial disease is suspected.

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Increased CSF F ₂ -isoprostane concentration in probable AD

Abstract: Increased CSF F2-isoprostanes are not an inevitable consequence of neurodegeneration and suggest that increased brain oxidative damage may occur early in the course of AD.

Cited by 236 publications

References 9 publications

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Clinical Characterization of a Familial Degenerative Myelopathy in Pembroke Welsh Corgi Dogs

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Increased CSF F 2 -isoprostane concentration in probable AD

Abstract: Increased CSF F2-isoprostanes are not an inevitable consequence of neurodegeneration and suggest that increased brain oxidative damage may occur early in the course of AD.

Cited by 236 publications

References 9 publications

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Clinical Characterization of a Familial Degenerative Myelopathy in Pembroke Welsh Corgi Dogs

Contact Info

Product

Resources

About

Increased CSF F ₂ -isoprostane concentration in probable AD