A soluble tau fragment generated by caspase-2 is associated with dementia in Lewy body disease
暂无分享,去创建一个
K. Ashe | C. Keene | Benjamin R. Smith | Kathryn M Nelson | Lisa J. Kemper | Kailee Leinonen-Wright | Benjamin Smith | Ashley Petersen
[1] Sonja W. Scholz,et al. Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study , 2018, The Lancet Neurology.
[2] A. Fagan,et al. ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy , 2017, Nature.
[3] C. Jack,et al. MAPT haplotype H1G is associated with increased risk of dementia with Lewy bodies , 2016, Alzheimer's & Dementia.
[4] Keith A. Johnson,et al. Tau Positron Emission Tomographic Imaging in the Lewy Body Diseases. , 2016, JAMA neurology.
[5] K. Zahs,et al. Caspase-2 cleavage of tau reversibly impairs memory , 2016, Nature Medicine.
[6] D. Allsop,et al. Effects of different isoforms of apoE on aggregation of the α‐synuclein protein implicated in Parkinson’s disease , 2016, Neuroscience Letters.
[7] M. Tiwari,et al. Caspase-2 resides in the mitochondria and mediates apoptosis directly from the mitochondrial compartment , 2016, Cell Death Discovery.
[8] L. Greene,et al. Caspase-2 Is Essential for C-jun Transcriptional Activation and Bim Induction in Neuron Death Nih Public Access Author Manuscript Proteins Were Detected Using Either Enhanced Chemiluminescence , 2022 .
[9] C. Bouras,et al. Neuropathology of dementia in a large cohort of patients with Parkinson's disease. , 2013, Parkinsonism & related disorders.
[10] J. Pozueta,et al. Caspase-2 is required for dendritic spine and behavioral alterations in J20 APP transgenic mice , 2013, Nature Communications.
[11] Daniel Weintraub,et al. APOE ε4 increases risk for dementia in pure synucleinopathies. , 2013, JAMA neurology.
[12] M. Nalls,et al. A large study reveals no association between APOE and Parkinson's disease , 2012, Neurobiology of Disease.
[13] D. Ehrnhoefer,et al. Mice lacking caspase-2 are protected from behavioral changes, but not pathology, in the YAC128 model of Huntington disease , 2011, Molecular Neurodegeneration.
[14] A. Di Polo,et al. Ocular neuroprotection by siRNA targeting caspase-2 , 2011, Cell Death and Disease.
[15] M. Tiwari,et al. A knockout of the caspase 2 gene produces increased resistance of the nigrostriatal dopaminergic pathway to MPTP-induced toxicity , 2011, Experimental Neurology.
[16] J. Kulisevsky,et al. Dementia risk in Parkinson disease: disentangling the role of MAPT haplotypes. , 2011, Archives of neurology.
[17] K. Ashe,et al. Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration , 2010, Neuron.
[18] M. Ban,et al. Tau and α‐synuclein in susceptibility to, and dementia in, Parkinson's disease , 2007 .
[19] Arlan Richardson,et al. Caspase-2 deficiency enhances aging-related traits in mice , 2007, Mechanisms of Ageing and Development.
[20] S. Srinivasula,et al. Oligomerization Is a General Mechanism for the Activation of Apoptosis Initiator and Inflammatory Procaspases* , 2003, The Journal of Biological Chemistry.
[21] J. Perlmutter,et al. Parkinson's disease and apolipoprotein E: possible association with dementia but not age at onset. , 2002, Genomics.
[22] S. Rabacchi,et al. Caspase-2 Mediates Neuronal Cell Death Induced by β-Amyloid , 2000, The Journal of Neuroscience.
[23] S. Shimohama,et al. Changes in caspase expression in Alzheimer's disease: comparison with development and aging. , 1999, Biochemical and biophysical research communications.
[24] Hilde van der Togt,et al. Publisher's Note , 2003, J. Netw. Comput. Appl..
[25] S. Rabacchi,et al. Caspase-2 mediates neuronal cell death induced by beta-amyloid. , 2000, The Journal of neuroscience : the official journal of the Society for Neuroscience.