- Aberrant tau phosphorylation by glycogen synthase kinase-3beta and JNK3 induces oligomeric tau fibrils in COS-7 cells
Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 351 0198, Japan
J Biol Chem 277:42060-5. 2002
..These results suggest that aberrant tau phosphorylation by the combination of these kinases may be involved in "pretangle," oligomeric tau fibril formation in vivo...
- Alterations in glucose metabolism induce hypothermia leading to tau hyperphosphorylation through differential inhibition of kinase and phosphatase activities: implications for Alzheimer's disease
Laboratory for Alzheimer s Disease, The Institute of Physical and Chemical Research, Wako Shi, Saitama 351 0198, Japan
J Neurosci 24:2401-11. 2004
..Our results imply that serine-threonine protein phosphatase 2A plays a major role in regulating tau phosphorylation in the adult brain and provide in vivo evidence for its crucial role in abnormal tau hyperphosphorylation in AD...
- A neuronal microtubule-interacting agent, NAPVSIPQ, reduces tau pathology and enhances cognitive function in a mouse model of Alzheimer's disease
Department of Neurology, Georgetown University Medical Center, 4000 Reservoir Road N W, Washington, DC 20057, USA
J Pharmacol Exp Ther 325:146-53. 2008
..Our results suggest that neuronal microtubule interacting agents such as NAP may be useful therapeutic agents for the treatment or prevention of tauopathies...
- Interplay between cyclin-dependent kinase 5 and glycogen synthase kinase 3 beta mediated by neuregulin signaling leads to differential effects on tau phosphorylation and amyloid precursor protein processing
Taub Institute at Columbia University Medical Center, New York State Psychiatric Institute, New York, New York 10032, USA
J Neurosci 28:2624-32. 2008
..Thus, cdk5 inhibitors may not be effective in targeting tau phosphorylation in the elderly...
- Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processing
Taub Institute at Columbia University Medical Center, New York, NY 10032, USA
Neuron 57:680-90. 2008
..These data demonstrate a pathway by which p25/cdk5 increases the amyloidogenic processing of APP through STAT3-mediated transcriptional control of BACE1 that could have implications for AD pathogenesis...
- Deregulation of protein phosphatase 2A and hyperphosphorylation of τ protein following onset of diabetes in NOD mice
Marie Amélie Papon
Centre hospitalier de l Universite Laval, Axe Neurosciences, Quebec, Canada
Diabetes 62:609-17. 2013
..This model may be a useful tool to address further mechanistic association between insulin dysfunction and AD pathology...
- Insulin dysfunction induces in vivo tau hyperphosphorylation through distinct mechanisms
Laboratory for Alzheimer s Disease, The Institute of Physical and Chemical Research, Saitama 351 0198, Japan
J Neurosci 27:13635-48. 2007
- Anesthesia leads to tau hyperphosphorylation through inhibition of phosphatase activity by hypothermia
Columbia University Medical Center, Department of Pathology, Taub Institute for Alzheimer s Disease Research, New York, New York 10032, USA
J Neurosci 27:3090-7. 2007
..Furthermore, a thorough examination of the effect of anesthesia-induced hypothermia on the risk and progression of AD is warranted...
- Anesthesia-induced hyperphosphorylation detaches 3-repeat tau from microtubules without affecting their stability in vivo
Taub Institute for Alzheimer s Disease Research, Department of Pathology, Columbia University Medical Center, New York, New York 10032, USA
J Neurosci 28:12798-807. 2008
..Tau remaining on the MTs under these conditions is sufficient to maintain MT network integrity...
- c-jun N-terminal kinase hyperphosphorylates R406W tau at the PHF-1 site during mitosis
Laboratory for Alzheimer s Disease, Brain Science Institute, The Institute of Physical and Chemical Research RIKEN, Saitama, Japan
FASEB J 20:762-4. 2006
- A transgenic rat that develops Alzheimer's disease-like amyloid pathology, deficits in synaptic plasticity and cognitive impairment
Department of Pathology, Taub Institute for Research on Alzheimer s Disease, Columbia University, Black Building 5 513, 650 West 168th Street, New York, NY 10032, USA
Neurobiol Dis 31:46-57. 2008
- Tau filament formation and associative memory deficit in aged mice expressing mutant (R406W) human tau
Laboratory for Alzheimer s Disease and Neural Architecture, Brain Science Institute, Institute of Physical and Chemical Research RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 351 0198, Japan
Proc Natl Acad Sci U S A 99:13896-901. 2002
- Retromer deficiency observed in Alzheimer's disease causes hippocampal dysfunction, neurodegeneration, and Abeta accumulation
Taub Institute for Research on Alzheimer s Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Proc Natl Acad Sci U S A 105:7327-32. 2008
..By recapitulating features of the disease, these animal models suggest that retromer deficiency observed in late-onset Alzheimer's disease can contribute to disease pathogenesis...
- Metabolic activity determines efficacy of macroautophagic clearance of pathological oligomeric alpha-synuclein
Wai Haung Yu
Dept of Pathology, Columbia University Medical Center, 630 W168th St Rm 12 461, New York NY 10032, USA
Am J Pathol 175:736-47. 2009
..This study provides therapeutic and pathological implications for both synucleinopathy and Parkinson's disease, identifying conditions in which autophagy may be insufficient to degrade alpha-syn aggregates...
- Propofol directly increases tau phosphorylation
Robert A Whittington
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York, United States of America
PLoS ONE 6:e16648. 2011
- In vivo turnover of tau and APP metabolites in the brains of wild-type and Tg2576 mice: greater stability of sAPP in the beta-amyloid depositing mice
Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
PLoS ONE 4:e7134. 2009
..Given the neurotrophic roles attributed to sAPP, the enhanced stability of sAPP in the beta-amyloid depositing Tg2576 mice may represent a neuroprotective response...
- Tau aggregates: toxic, inert, or protective species?
Columbia University Medical Center, Taub Institute for Research on Alzheimer s Disease and the Aging Brain, New York, NY 10032, USA
J Alzheimers Dis 14:431-6. 2008
..Here, we will first examine tau aggregation and its putative roles in Alzheimer's disease. We will then review the findings concerning different species of tau and their potential toxicity...
- Acceleration and persistence of neurofibrillary pathology in a mouse model of tauopathy following anesthesia
Axe Neurosciences, Centre hospitalier de l Universite Laval, Universite Laval, Quebec, Quebec, Canada
FASEB J 23:2595-604. 2009
- Hypothermia and Alzheimer's disease neuropathogenic pathways
R A Whittington
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, 622 West 168th Street PH 5, New York, NY 10032, USA
Curr Alzheimer Res 7:717-25. 2010
..Here, we review the preclinical data involving hypothermia with tau and Aβ, as well as clinical evidence implicating hypothermia in the development of AD...
- Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo
Center for Dementia Research, Nathan S Kline Institute, New York University, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Proc Natl Acad Sci U S A 102:6990-5. 2005
..These results support the idea that kinases are involved in tauopathy progression and that kinase inhibitors may be effective therapeutically...
- U-box protein carboxyl terminus of Hsc70-interacting protein (CHIP) mediates poly-ubiquitylation preferentially on four-repeat Tau and is involved in neurodegeneration of tauopathy
Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Fukuoka, Japan
J Neurochem 91:299-307. 2004
..Thus, CHIP is a ubiquitin ligase for four-repeat tau and maintains neuronal survival by regulating the quality control of tau in neurons...
- Untangling memory deficits
Nat Med 11:826-7. 2005