scispace - formally typeset
Search or ask a question

Showing papers by "Michael T. Lin published in 2006"


Journal ArticleDOI
19 Oct 2006-Nature
TL;DR: Treatments targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria hold great promise in ageing-related neurodegenerative diseases.
Abstract: Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.

5,368 citations


Journal ArticleDOI
TL;DR: Serum and brain creatine concentrations increased in the creatine-treated group and returned to baseline after washout, and serum 8-hydroxy-2′-deoxyguanosine levels, an indicator of oxidative injury to DNA, levels were markedly elevated in HD and reduced by creatine treatment.
Abstract: In a randomized, double-blind, placebo-controlled study in 64 subjects with Huntington disease (HD), 8 g/day of creatine administered for 16 weeks was well tolerated and safe. Serum and brain creatine concentrations increased in the creatine-treated group and returned to baseline after washout. Serum 8-hydroxy-2'-deoxyguanosine (8OH2'dG) levels, an indicator of oxidative injury to DNA, were markedly elevated in HD and reduced by creatine treatment.

305 citations


Journal ArticleDOI
TL;DR: New findings in humans examine how mitochondrial function declines during Alzheimer disease and how this decline is driven by age, disease and environmental factors.
Abstract: New findings in humans examine how mitochondrial function declines during Alzheimer disease

136 citations


Journal ArticleDOI
TL;DR: Treated LGG patients had lower scores than untreated patients on several cognitive domains; patients who completed treatment at intervals greater than 3 years and had long disease duration had significantly lower scores on the Non-Verbal Memory domain.
Abstract: Background The role of radiotherapy and chemotherapy in the treatment of low-grade gliomas (LGG) is controversial regarding their effect on survival and the development of neurotoxicity. The few published studies examining adverse treatment effects on cognition revealed conflicting results.

89 citations


Journal ArticleDOI
TL;DR: It is concluded that the Ca0 and Kd values of the BK channel can be modulated by differential channel phosphorylation, which can be explained by a greater extent of channelosphorylation of fetal than adult myocytes.
Abstract: Large-conductance Ca2+-sensitive K+ (BK) channel activity is greater in basilar artery smooth muscle cells (SMCs) of the fetus than the adult, and this increased activity is associated with a lower...

30 citations