18 RESULTS
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COMMENT Those working and playing with Mark had a special knowledge, the secret of his superhuman power to get things done. It was simple: generosity of spirit, intellect and effort, all hidden under a legendary sense of humor and love of life. Mark supported ...
COMMENT Comment by George Perry, Rudy J. Castellani, and Mark A. Smith Failure of Amyloid-β-based Therapeutics: Is Amyloid the Culprit or the Savior? The failure of the amyloid-β-based therapeutic, semagacestat, to benefit patients suffering from Alzheimer ...
COMMENT Mitochondria in Alzheimer Disease: Pulling the Plug on the Synapse Zheng Li and colleagues provide compelling data and discussion to confirm the growing suspicion that proper mitochondrial structure and function are requisite for synaptic operation. ...
COMMENT Leaping on Leptin: What’s the Skinny? The work by Fewlass and colleagues [1] provides an impressive array of data suggesting that leptin hormone homeostasis and/or dysregulation bears upon the metabolism of amyloid-β (Aβ). Although not confirmed by ...
COMMENT Caspase Activation But Not Apoptosis The article by Rissman and colleagues (2004) and accompanying commentary by Dickson (2004) highlight the potential importance of caspase activation in Alzheimer disease (AD). In the former, Rissmann et al. (2004) ...
COMMENT Brain Aging and Age-Related Neurodegenerative Diseases: Are Vitamin and Trace-element Supplementation the "Miraculous" Solution? Alzheimer’s disease (AD) is a common and complex neurodegenerative disease that affects approximately 15 million ...
COMMENT DNA Damage Mediated Cell Cycle Reentry in AD The search to elucidate pathologic mechanisms of neuronal death in Alzheimer's disease has demonstrated that dysregulation of two major cellular processes—cell cycle control and response pathways to ...
COMMENT Bonifati and colleagues bring genetic evidence of oxidative imbalance to the field of Parkinson’s disease research. In light of the abundant biochemical data demonstration nitration (Good et al., 1998; Giasson et al., 2002), lipid peroxidation and ...
COMMENT Eat Less, Live More —But Why? Comment by George Perry and Mark A. Smith Institute of Pathology, Case Western Reserve University, Cleveland, Ohio USA A well lived life can only be seen in retrospect of a lifetime of living and, in the view of the ancient ...
COMMENT Harlequin and Alzheimer Disease: Remarkable Parallels If it takes years to die, it is not by an apoptotic mechanism. Klein and colleagues (2002) present an excellent model for this assertion and a couple of other phenomena that are present in Alzheimer ...
COMMENT Pathogenic versus Pathology Voigtlander and colleagues provide compelling supporting evidence for the notion that PrP is a neuroprotectant. Therefore, PrP, like amyloid-beta protein precursor/amyloid-beta in Alzheimer disease (AD), alpha-synuclein in ...
COMMENT Stalling the Ravages of Aging (and Alzheimer's?) With Antioxidants "Since its conception nearly 50 years ago (Harman, 1956), the free radical theory of aging has found some of its best support from studies of brain aging and Alzheimer disease ...
COMMENT Mitochondria, Amyloid-β, and Metabolism Studies of amyloid-β (Aβ) cellular toxicity using cells with the full complement of organelles have implicated various sites of action but have primarily focused on the plasma membrane (Mark et al., 1997). Indeed, ...
COMMENT Oxidative Abnormalities As The Earliest Changes In Amyloid-b Disease Determining the chronological and mechanistic interrelationship of Alzheimer disease (AD) is critical to both elucidating its etiology and developing efficacious therapeutics that are ...
COMMENT Interventions to modify oxidant balance to provide protection from Alzheimer disease (AD) are as hotly debated as it has been for other age-related diseases. In recent studies (Engelhart et al., Foley and White, Morris, et al.), dietary intake of vitamin ...
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