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Open AccessJournal ArticleDOI

Age-related losses of cognitive function and motor skills in mice are associated with oxidative protein damage in the brain.

TLDR
The results support the view that oxidative stress is a causal factor in brain senescence and suggest that age-related declines of cognitive and motor performance progress independently, and involve oxidative molecular damage within different regions of the brain.
Citations
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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.
Journal ArticleDOI

Biochemistry and pathology of radical-mediated protein oxidation

TL;DR: Proteins are also key targets in defensive cytolysis and in inflammatory self-damage, and the possibility of selective protection against protein oxidation (antioxidation) is raised.
Journal ArticleDOI

Role of free radicals in the neurodegenerative diseases: therapeutic implications for antioxidant treatment.

TL;DR: Little is known about the impact of dietary antioxidants upon the development and progression of neurodegenerative diseases, especially Alzheimer’s disease, but there are many attempts to develop antioxidants that can cross the blood-brain barrier and decrease oxidative damage.
Journal ArticleDOI

Caloric Intake and Aging

TL;DR: In postindustrial societies, overeating, inactivity, and obesity have emerged as new challenges in public health and considerable effort is now being devoted to determining the pathophysiologic causes of these problems.
Journal ArticleDOI

The mitochondrial energy transduction system and the aging process.

TL;DR: Dysfunctional mitochondria in aged rodents are characterized, besides decreased electron transfer and O(2) uptake, by an increased content of oxidation products of phospholipids, proteins and DNA, a decreased membrane potential, and increased size and fragility.
References
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Book ChapterDOI

Determination of carbonyl content in oxidatively modified proteins.

TL;DR: This chapter discusses methods to determine carbonyl content in oxidatively modified proteins and quantitated protein-bound pyruvoyl groups through formation of a Schiff base with p-aminobenzoic acid followed by reduction with cyanoborohydride.
Journal ArticleDOI

Oxidative stress, glutamate, and neurodegenerative disorders

TL;DR: Two broad mechanisms--oxidative stress and excessive activation of glutamate receptors--are converging and represent sequential as well as interacting processes that provide a final common pathway for cell vulnerability in the brain.
Journal ArticleDOI

Reactive Oxygen Species and the Central Nervous System

TL;DR: The nature of antioxidants is discussed, it being suggested that antioxidant enzymes and chelators of transition metal ions may be more generally useful protective agents than chain‐breaking antioxidants.
Journal ArticleDOI

On the role of the hippocampus in learning and memory in the rat

TL;DR: The general finding that rats without a hippocampus were impaired on those tasks that required the utilization of spatial and contextual information stands in contrast with the spared performance that was found in learning about and handling (even complex) nonspatial information.
Journal ArticleDOI

Oxidative damage, mitochondrial oxidant generation and antioxidant defenses during aging and in response to food restriction in the mouse

TL;DR: Mechanisms of aging and life span shortening by enhanced caloric intake are associated with oxidative damage arising from corresponding changes in mitochondrial oxidant production and protein carbonyl content, and mitochondrial O2.- and H2O2 generation may act as indices of aging.
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