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COMMENT This is an outstanding study. It not only adds significant evidence supporting a critical role of mitochondrial dysfunction in the pathogenesis of Alzheimer’s disease, but also specifically suggests mitophagy as a promising therapeutic target for AD. ...
COMMENT Mitochondrial dysfunction is one of the most prominent and earliest deficits in Alzheimer's and likely plays a critical role in the pathogenesis of this disease. This interesting study demonstrated a novel mechanism by which Aβ causes mitochondrial ...
COMMENT A Critical Role of Mitochondrial Dynamics in the Pathogenesis of AD Dr. Feany and colleagues should be congratulated for an elegant Drosophila genetic study. They convincingly demonstrated that tau overexpression causes mitochondrial elongation in ...
COMMENT This is a very well-executed study with very careful and detailed measurement of mitochondrial morphology and transport in motor neurons in an ALS model, and which extends the authors’ previous findings (Magrané et al., 2009). Mitochondrial Dendra is a ...
COMMENT It is increasingly accepted that abnormal mitochondrial dynamics likely underlie mitochondrial dysfunction in AD. Despite some discrepancy with the prior publications from our group, this is an interesting paper that adds important in vivo evidence ...
COMMENT Evading Apoptosis in Alzheimer Disease Comment by Baiyang Sheng, Hyoung-gon Lee, George Perry, Mark A. Smith, Xiongwei Zhu Using multiphoton live brain imaging in a mouse model of Alzheimer disease (AD), Hyman and colleagues were able to investigate the ...
COMMENT Comment by Hyoung-gon Lee, Xiongwei Zhu, Xinglong Wang, Rudy J. Castellani, George Perry, and Mark A. Smith Cancer, Alzheimer Disease, and Cardiovascular Disease: Associations and Disassociations—Clues to Etiology? There are numerous pathological ...
COMMENT Synaptic loss and mitochondrial dysfunction are both early features of Alzheimer disease, and connecting the two, as demonstrated in several recent studies including this present work, is attractive. Our recent work revealed that mitochondria accumulate ...
COMMENT Uric Acid: Not Just for Gout Anymore The major flaw of the antioxidant theory of aging is the lack of efficacy of antioxidant supplements against diseases of aging. A patchwork of experimental demonstrations show that oxidative stress is involved in ...
COMMENT Strengthening the Links Between Amyloid-β, Mitochondria and Oxidative Stress Striking features of Alzheimer disease pathophysiology are amyloid-β deposits, reduced brain metabolism, oxidative stress, and cognitive decline. The links between these features ...
COMMENT To explore the mechanisms underlying nitric oxide- and Aβ-induced mitochondrial fragmentation in neurons (Barsoum et al., 2006), Stuart Lipton’s group convincingly demonstrates that NO induces S-nitrosylation of Drp1 at Cys644 that enhances Drp1 ...
COMMENT Comment by Rudy J. Castellani, George Perry, Xiongwei Zhu, Hyoung-gon Lee, Mark A. Smith The Next Phase: Prevention. Where Do I Sign Up? The Aβ vaccination strategy failed because it was not used early enough in the course of the disease. Come again? We ...
COMMENT Comment by Rudy J. Castellani, George Perry, Xiongwei Zhu, Hyoung-gon Lee, Mark A. Smith 1911 to 2008: The Dismal Progress of Knowledge in Alzheimer’s Disease Research In a study of senile plaques in brains of the demented and non-demented, Fuller in 1911 ...
COMMENT Amyloid Spin Doctors It certainly would seem that the Alzheimer disease (AD) research community has completed the 180-degree turnaround on their view of the toxic amyloid-β entity, i.e., from fibrils to oligomers. The days of plaque busters are presumably ...
COMMENT Antioxidant Defenses—Nitric Oxide, Amyloid-β and Tau Phosphorylation: A Zero Sum Game This paper is exceptionally well executed and may lead to a paradigm shift. Dogma indicates that nitric oxide, amyloid-β, and tau phosphorylation are all bad. By ...
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