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| 1 | GSK-3beta in- hibition reverses axonal transport defects and behavioural phe- notypes in Drosophila显示文摘 | Mudher A Shepherd D Newman T A | 2004 | Mol Psychiatry2004，9，5： | 1 |
| 2 | Total reflection X-ray fluorescence: A technique for trace element analysis in materials 显示文摘 | Misra N L Mudher K D S | 2002 | Progress in Crystal Growth and Characterization of Materials2002，6574，： | 1 |
| 3 | Alzheimer’s disease do tauists and baptistsfinally shake hands-显示文摘 | Mudher A Lovestone S | 2002 | Trends Neurosci2002，25，1： | 1 |
| 4 | GSK-3beta inhibition reverses axonal transport defects and behavioural phenotypes in Drosophila显示文摘 | Mudher A Shepherd D Newman TA | | 0，，： | 1 |
| 5 | Alzheimer's disease-do tanists and baptists finally shake hands? 显示文摘 | Mudher A Lovestone S | 2002 | Trends Neurosci2002，25，： | 1 |
| 6 | Alzheimers disease - do tauists and baptists finally shake hands? 显示文摘 | Mudher A Lovestone S | 2002 | Trends Neurosci2002，25，1： | 1 |
| 7 | Dishevelled regulates the metabolism of amyloid precursor protein via proter kinase C/mitogen-activated protein kinase and c-Jun teminal kinase显示文摘 | MUDHER A CHAPMAN S RICHARDSON J | 2001 | J Neurosci2001，21，14： | 1 |
| 8 | Are tau aggregates toxic or protective in tauopathies? 显示文摘 | Cowan C M Mudher A | 2013 | Front Neurol2013，4，： | 1 |
| 9 | Structural and thermal studies on Na2 Th ( MoO4 ) 3, Na2 Pu ( MoO4 ) 3, Na4 Th (MOO4)4 and Na4Pu(MoO4)4显示文摘 | Dahale N D Meera Keskar Singh Mudher K D | 2006 | Journal of Alloys and Com- pounds2006，415，12： | 1 |
| 10 | Current Challenges and Controversies in Drug-Induced Liver Injury显示文摘 | Corsini Alberto Ganey Patricia Ju Cynthia Kaplowitz Neil Pessayre Dominique Roth Robert Watkins Paul B Albassam Mudher Liu Baolian Stancic Saray Suter Laura Bortolini Michele | 2012 | Drug Safety2012，，12： | 1 |
| 11 | Dishevelled regulates the metabolism of amyloid precursor protein via protein kinase C/mitogen-activated protein kinase and c-Jun terminal kinase显示文摘 | Mudher A Chapman S Richardson J | 2001 | J Neurosci2001，21，14： | 1 |
| 12 | Necrotizing fasciitis: a challenging diagnosis显示文摘 | Ashraf F. Hefny Hani O. Eid Mudher Al-Hussona Kamal M. Idris Fikri M. Abu-Zidan | 2007 | European Journal of Emergency Medicine2007，，1： | 1 |
| 13 | Alzheimer's disease-do tauists and baptists finally shake hands显示文摘 | Mudher A Lovestone S | 2002 | Trends in Neurosciences2002，25，1： | 1 |
| 14 | Alzheimer's disease-do tauists and baptists finally shake hands显示文摘 | MUDHER A LOVESTONE S | 2002 | Trends in Neurosciences2002，25，1： | 1 |
| 15 | How do neurons age?A focused review on the aging of the microtubular cytoskeleton显示文摘Aging is the leading risk factor for Alzheimer’s disease and other neurodegenerative diseases. We now understand that a breakdown in the neuronal cytoskeleton, mainly underpinned by protein modifications leading to the destabilization of microtubules, is central to the pathogenesis of Alzheimer’s disease. This is accompanied by morphological defects across the somatodendritic compartment, axon, and synapse. However, knowledge of what occurs to the microtubule cytoskeleton and morphology of the neuron during physiological aging is comparatively poor. Several recent studies have suggested that there is an age-related increase in the phosphorylation of the key microtubule stabilizing protein tau, a modification, which is known to destabilize the cytoskeleton in Alzheimer’s disease. This indicates that the cytoskeleton and potentially other neuronal structures reliant on the cytoskeleton become functionally compromised during normal physiological aging. The current literature shows age-related reductions in synaptic spine density and shifts in synaptic spine conformation which might explain age-related synaptic functional deficits. However, knowledge of what occurs to the microtubular and actin cytoskeleton, with increasing age is extremely limited. When considering the somatodendritic compartment, a regression in dendrites and loss of dendritic length and volume is reported whilst a reduction in soma volume/size is often seen. However, research into cytoskeletal change is limited to a handful of studies demonstrating reductions in and mislocalizations of microtubule-associated proteins with just one study directly exploring the integrity of the microtubules. In the axon, an increase in axonal diameter and age-related appearance of swellings is reported but like the dendrites, just one study investigates the microtubules directly with others reporting loss or mislocalization of microtubule-associated proteins. Though these are the general trends reported, there are clear disparities between model organisms and brain regions that are worthy of further investigation. Additionally, longitudinal studies of neuronal/cytoskeletal aging should also investigate whether these age-related changes contribute not just to vulnerability to disease but also to the decline in nervous system function and behavioral output that all organisms experience. This will highlight the utility, if any, of cytoskeletal fortification for the promotion of healthy neuronal aging and potential protection against age-related neurodegenerative disease. This review seeks to summarize what is currently known about the physiological aging of the neuron and microtubular cytoskeleton in the hope of uncovering mechanisms underpinning age-related risk to disease. | Brad Richardson Thomas Goedert Shmma Quraishe Katrin Deinhardt Amritpal Mudher | 2024 | Neural Regeneration Research2024，19，9： | 0 |
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