Simon Melov

'...and C is for Clioquinol' - the AbetaCs of Alzheimer's disease.

Applied proteomics: mitochondrial proteins and effect on function.

Therapeutics against mitochondrial oxidative stress in animal models of aging.

Animal models of oxidative stress, aging, and therapeutic antioxidant interventions.

Microarray workshop on aging.

Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts.

Oxidative stress and aging: beyond correlation.

Spotlight on nematode mitochondria in RNAi mega-screen.

Endogenous mitochondrial oxidative stress: neurodegeneration, proteomic analysis, specific respiratory chain defects, and efficacious antioxidant therapy in superoxide dismutase 2 null mice.

Microarray analysis of gene expression with age in individual nematodes.

Microscale fractionation facilitates detection of differentially expressed proteins in Alzheimer's disease brain samples.

Modeling mitochondrial function in aging neurons.

Proteomic analysis of mitochondrial proteins.

Microarrays as a tool to investigate the biology of aging: a retrospective and a look to the future.

Mice transgenic for Alzheimer disease beta-amyloid develop lens cataracts that are rescued by antioxidant treatment.

Pharmacogenomic profiling of an oxidative stress-mediated spongiform encephalopathy.

Hyperplasia, reduced E-cadherin expression, and developmental arrest in mammary glands oxidatively stressed by loss of mitochondrial superoxide dismutase.

Gene expression profiling in mitochondrial disease: assessment of microarray accuracy by high-throughput Q-PCR.

Alzheimer disease beta-amyloid activity mimics cholesterol oxidase.

Biomarker discovery and analysis platform: application to Alzheimer's disease.

Science fact and the SENS agenda. What can we reasonably expect from ageing research?

Mitochondrial reactive oxygen species in mice lacking superoxide dismutase 2: attenuation via antioxidant treatment.

Pol II-expressed shRNA knocks down Sod2 gene expression and causes phenotypes of the gene knockout in mice.

Nigrostriatal dopaminergic neurodegeneration in the weaver mouse is mediated via neuroinflammation and alleviated by minocycline administration.

Dramatic age-related changes in nuclear and genome copy number in the nematode Caenorhabditis elegans.

Resistance exercise reverses aging in human skeletal muscle.

Mitochondrial oxidative stress causes hyperphosphorylation of tau.

Global and targeted gene expression and protein content in skeletal muscle of young men following short-term creatine monohydrate supplementation.

Pharmacogenetic analysis of lithium-induced delayed aging in Caenorhabditis elegans.

Gene expression changes associated with aging in C. elegans.

Age-related behaviors have distinct transcriptional profiles in Caenorhabditis elegans.

Increase in mitochondrial biogenesis, oxidative stress, and glycolysis in murine lymphomas.

A human protein interaction network shows conservation of aging processes between human and invertebrate species.

Limb immobilization induces a coordinate down-regulation of mitochondrial and other metabolic pathways in men and women.

Eccentric exercise activates novel transcriptional regulation of hypertrophic signaling pathways not affected by hormone changes.

Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans.

Impaired spare respiratory capacity in cortical synaptosomes from Sod2 null mice.

The garlic constituent diallyl trisulfide increases the lifespan of C. elegans via skn-1 activation.

Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice.

Loss of intestinal nuclei and intestinal integrity in aging C. elegans.

Life span extension via eIF4G inhibition is mediated by posttranscriptional remodeling of stress response gene expression in C. elegans.

Cellular senescence: a link between cancer and age-related degenerative disease?

On the programmed/non-programmed nature of ageing within the life history.

Human embryonic stem cells express elevated levels of multiple pro-apoptotic BCL-2 family members.

Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin.

Massage therapy attenuates inflammatory signaling after exercise-induced muscle damage.