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Journal ArticleDOI

Modeling mitochondrial function in aging neurons.

Simon Melov
- 01 Oct 2004 - 
- Vol. 27, Iss: 10, pp 601-606
TLDR
This review will highlight several new animal models of mitochondrial dysfunction in the context of aging by highlighting the importance of mitochondria-mediated pathophysiology in aging.
About
This article is published in Trends in Neurosciences.The article was published on 2004-10-01. It has received 122 citations till now. The article focuses on the topics: Steroid biosynthesis & Respiratory chain.

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Citations
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Journal ArticleDOI

Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer's Disease

TL;DR: DLP1 overexpression, likely through repopulation of neuronal processes with mitochondria, prevented ADDL-induced synaptic loss, suggesting that abnormal mitochondrial dynamics plays an important role in ADDL -induced synaptic abnormalities.
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The hubs of the human connectome are generally implicated in the anatomy of brain disorders

TL;DR: Using network analysis of DTI data from healthy volunteers, and meta-analyses of published MRI studies in 26 brain disorders, Crossley et al. show that lesions across disorders tend to be concentrated at hubs.
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Ageing and neuronal vulnerability

TL;DR: Emerging evidence on protein interaction networks that monitor and respond to the normal ageing process suggests that successful neural ageing is possible for most people, but also cautions that cures for neurodegenerative disorders are unlikely in the near future.
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Ageing and the brain.

TL;DR: Protective factors that reduce cardiovascular risk, namely regular exercise, a healthy diet, and low to moderate alcohol intake, seem to aid the ageing brain as does increased cognitive effort in the form of education or occupational attainment.
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Discovering statistically significant pathways in expression profiling studies

TL;DR: A statistical framework for determining whether a specified group of genes for a pathway has a coordinated association with a phenotype of interest is proposed, and it is shown that the differences in the correlation structure of each set of genes can lead to a biased comparison among gene sets unless a normalization procedure is applied.
References
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Journal ArticleDOI

The Free Radical Theory of Aging Matures

TL;DR: The status of the free radical theory of aging is reviewed, by categorizing the literature in terms of the various types of experiments that have been performed, which include phenomenological measurements of age-associated oxidative stress, interspecies comparisons, dietary restriction, and the ongoing elucidation of the role of active oxygen in biology.
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Neurodegenerative diseases and oxidative stress.

TL;DR: Oxidative stress has been implicated in the progression of Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis and different strategies, including novel metal–protein attenuating compounds aimed at a variety of targets have shown promise in clinical studies.
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Premature ageing in mice expressing defective mitochondrial DNA polymerase

TL;DR: The results provide a causative link between mtDNA mutations and ageing phenotypes in mammals by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase.
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Dilated Cardiomyopathy and Neonatal Lethality in Mutant Mice Lacking Manganese Superoxide Dismutase

TL;DR: Cytochemical analysis revealed a severe reduction in succinate dehydrogenase and aconitase activities in the heart and, to a lesser extent, in other organs, which indicates that MnSOD is required for normal biological function of tissues by maintaining the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide.
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Mitochondrial genetics: a paradigm for aging and degenerative diseases?

TL;DR: Application of the hypothesis that a variety of degenerative processes may be associated with defects in oxidative phosphorylation has provided new insights into such diverse clinical problems as ischemic heart disease, late-onset diabetes, Parkinson's Disease, Alzheimer's disease, and aging.
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