Metals accelerate production of the aberrant splicing isoform of the presenilin‐2

Matsuzaki, Shinsuke; Manabe, Takayuki; Katayama, Taiichi; Nishikawa, Akio; Yanagita, Teruyoshi; Okuda, Hiromichi; Yasuda, Yuki; Miyata, Sumiko; Meshitsuka, Shunsuke; Tohyama, Masaya

doi:10.1111/j.1471-4159.2004.02290.x

Cited by 44 publications

(36 citation statements)

References 32 publications

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“…Metals, including aluminum, contribute to oxidative stress by playing a major catalytic role in the production of free radicals [36]. Tea catechins have been shown to complex with aluminum, and may repress aluminum absorption during tea intake [37].…”

Section: Tea Preparationsmentioning

confidence: 99%

Chemoprevention of lung cancer by tea

Clark

You²

2006

Molecular Nutrition Food Res

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Tea is the second only to water as the most consumed beverage in the world. Both green and black teas have been studied for their health benefits for a variety of diseases, particularly cancer. Lung cancer is the predominant cause of cancer mortality in developed countries. Smokers' risk of lung cancer is 20 times that of persons who have never smoked. Epidemiological studies on the cancer-preventive effects of tea produce inconsistent results, which could in part be attributed to the lack of a universal standard for tea preparations. However, most animal studies indicate that tea has strong chemopreventive effects against lung tumorigenesis. The reported mechanisms for chemopreventive activity of green tea are antioxidation, induction of phase II enzymes, inhibition of TNFalpha expression and release, inhibition of cell proliferation, and induction of apoptosis. Cell cycle arrest and apoptosis induced by green tea are probably the two most significant factors. Future studies are needed to determine how green tea affects the genes associated with cell cycle regulation and apoptosis during the mouse lung carcinogenesis process.

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Section: Tea Preparationsmentioning

confidence: 99%

Chemoprevention of lung cancer by tea

Clark

You²

2006

Molecular Nutrition Food Res

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“…The authors concluded that such differences do exist in response to a dietary aluminum challenges resulting in permeability of the BBB and subsequent differential loading of aluminum. Matsuzaki et al [163], reported that chronic Al exposure has accelerated PS2V (the aberrant splicing isoform generated by skipping exon 5 of the PS-2 gene) production through hypoxia mechanism. HMGA1a, a mediator of PS2V production was shown to be induced by Al as well as by hypoxia.…”

Section: Cross-talk Between Genetic Susceptibility and Al In Admentioning

confidence: 99%

Aluminium in Alzheimer?s disease: are we still at a crossroad?

Gupta

Anitha

Hegde

et al. 2005

CMLS, Cell. Mol. Life Sci.

276

145

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Aluminium, an environmentally abundant non-redox trivalent cation has long been implicated in the pathogenesis of Alzheimer's disease (AD). However, the definite mechanism of aluminium toxicity in AD is not known. Evidence suggests that trace metal homeostasis plays a crucial role in the normal functioning of the brain, and any disturbance in it can exacerbate events associated with AD. The present paper reviews the scientific literature linking aluminium with AD. The focus is on aluminium levels in brain, region-specific and subcellular distribution, its relation to neurofibrillary tangles, amyloid beta, and other metals. A detailed mechanism of the role of aluminium in oxidative stress and cell death is highlighted. The importance of complex speciation chemistry of aluminium in relation to biology has been emphasized. The debatable role of aluminium in AD and the cross-talk between aluminium and genetic susceptibility are also discussed. Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in AD cannot be discarded. However, whether aluminium is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood.

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“…The aberrant splicing isoform (PS2V) generated by skipping exon5 of the presenilin-2 (PS2) gene is a diagnostic feature of sporadic AD (SAD). It has been demonstrated that chronic exposure to aluminum accelerates PS2V production induced by hypoxia in human neuroblastoma cells [33]. PS2V has also been reported to cause significant increases in the production of both Ab 40 and Ab 42 [34].…”

Section: Discussionmentioning

confidence: 99%

“…For example, astrocytes have been shown to undergo an active process of apoptosis in Alzheimer's disease (AD) [31] and that this process may precede the death of neurons [32]. Moreover, chronic exposure to aluminum has been reported to accelerate the production of the aberrant splicing isoform of presenilin-2 (PS2V), a diagnostic feature of sporadic AD [33]. PS2V protein has also been found to affect the UPR and cause an increase in the production of both amyloid beta (Ab)-40 and Ab-42 [34].…”

Section: Introductionmentioning

confidence: 99%