Pathogenic theories and intrathecal analysis of the sporadic form of Alzheimer’s disease

Torreilles, François; Touchon, Jacques

doi:10.1016/s0301-0082(01)00030-2

Cited by 34 publications

(19 citation statements)

References 144 publications

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“…However, since PrP C has a SOD-1 like activity, and Aβ-peptide is known to induce oxidative stress [7], PrP C staining of Aβ-plaques may represent an anti-oxidant neuroprotective role for PrP C . The PrP staining of ependyma is also compatible with this hypothesis, since these cells are exposed to free radicals in the cerebrospinal fluid [8]. The immunohistochemical studies of Voigtlander et al [9] and Ferrer et al…”

supporting

confidence: 54%

Comment on ?The codon 129 polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects?

McNeill

2004

J Neurol

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supporting

confidence: 54%

Comment on ?The codon 129 polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects?

McNeill

2004

J Neurol

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“…Inflammatory processes play a key role in the pathogenesis of the degenerative changes associated with disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS) (Torreilles and Touchon, 2002;Munch et al, 2003). This is particularly well documented for AD and MS (LeVine, 1997), in which inflammatory reactions are associated with glial activation, complement proteins, and other indicators of inflammatory responses (Torreilles et al, 1999;Hoozemans et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Cytokine toxicity to oligodendrocyte precursors is mediated by iron

Zhang

Haaf

Todorich

et al. 2005

Glia

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Inflammatory processes play a key role in the pathogenesis of a number of common neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Abnormal iron accumulation is frequently noted in these diseases and compelling evidence exists that iron is involved in inflammatory reactions. Histochemical stains for iron repeatedly demonstrate that oligodendrocytes, under normal conditions, stain more prominently than any other cell type in the brain. Therefore, we examined the hypothesis that cytokine toxicity to oligodendrocytes is iron mediated. Oligodendrocytes in culture were exposed to interferon-gamma (IFN-gamma), interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha). Toxicity was observed in a dose-dependent manner for IFN-gamma and TNF-alpha. IL-1beta was not toxic in the concentrations used in this study. The toxic concentration of IFN-gamma, and TNF-alpha was lower if the cells were iron loaded, but iron loading had no effect on the toxicity of IL-1beta. These data provide insight into the controversy regarding the toxicity of cytokines to oligodendrocytes by revealing that iron status of these cells will significantly impact the outcome of cytokine treatment. The exposure of oligodendrocytes to cytokines plus iron decreased mitochondrial membrane potential but activation of caspase 3 is limited. The antioxidant, TPPB, which targets mitochondria, protected the oligodendrocytes from the iron-mediated cytotoxicity, providing further support that mitochondrial dysfunction may underlie the iron-mediated cytokine toxicity. Therapeutic strategies involving anti-inflammatory agents have met with limited success in the treatment of demyelinating disorders. A better understanding of these agents and the contribution of cellular iron status to cytokine toxicity may help develop a more consistent intervention strategy.

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“…Unusual behaviour is accompanied by three main structural changes in the brain including diffuse loss of neurons, intracellular protein deposits termed neurofibrillary tangles (NFT) consisting of hyperphosphorylated tau protein and extracellular protein deposits termed β-amyloid (Aβ) or senile plaques, surrounded by dystrophic neuritis [1–3]. …”

Section: Introductionmentioning

confidence: 99%

Experimental research Effects of berberine on β-secretase activity in a rabbit model of Alzheimer’s disease

Panahi¹,

Mahmoudian²,

Mortazavi³

et al. 2013

aoms

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IntroductionRelevant aspects of Alzheimer's disease (AD) can be modeled by aluminium-maltolate injection into specific regions of the brain. The possible role of berberine chloride (BC) as an anti-inflammatory agent in the brain has been previously addressed.Material and methodsRabbits were divided into control (C), untreated lesion (L) and BC-treated + lesion (L + BC) groups. Animals in L + BC received BC (50 mg/ kg) orally 1 day after surgery and daily for 2 weeks. The lesion was induced by injection of 100 µl of either vehicle or water containing 25 mM aluminium-maltol into intraventricular fissure. Weight loss, ataxia, paralysis and tremor were monitored. For histopathology, Bielschowsky silver and H&E staining were employed. β-Secretase activity in hippocampus was finally assessed.ResultsAll L animals died on days 12-15 after lesion. Seven to 10 days after lesion, abnormal symptoms as well as cachexia were seen in over 90% of cases. L rabbits lost an average of 0.5 kg which was significant on days 10 and 12 (p < 0.05); this was not completely prevented by BC. Up to day 15, all L animals had lost their lives (p < 0.001). BC treatment protected the hippocampus from degeneration, altered the behavior and decreased the activity of β-site amyloid precursor protein cleaving enzyme-1 (BACE-1).ConclusionsConsidering the findings in regard to physiological abilities, histological changes and BACE-1 activity in hippocampus changes, it is concluded that BC treatment could be an effective therapy in restoring Al maltol-induced behavioral derangements in the rabbit model of AD.

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Pathogenic theories and intrathecal analysis of the sporadic form of Alzheimer’s disease

Cited by 34 publications

References 144 publications

Comment on ?The codon 129 polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects?

Comment on ?The codon 129 polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects?

Cytokine toxicity to oligodendrocyte precursors is mediated by iron

Experimental research Effects of berberine on β-secretase activity in a rabbit model of Alzheimer’s disease

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