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M. Westerman, Deirdre Cooper-Blacketer, A. Mariash, L. Kotilinek, T. Kawarabayashi, L. Younkin, G. Carlson, S. Younkin, K. Ashe (2002)
The relationship between Abeta and memory in the Tg2576 mouse model of Alzheimer's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience, 22 5
G. Mckhann, D. Drachman, M. Folstein, R. Katzman, D. Price, E. Stadlan (1984)
Clinical diagnosis of Alzheimer's diseaseNeurology, 34
D. Morgan, D. Diamond, P. Gottschall, K. Ugen, C. Dickey, J. Hardy, K. Duff, P. Jantzen, G. Dicarlo, D. Wilcock, K. Connor, J. Hatcher, C. Hope, M. Gordon, G. Arendash (2000)
A beta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease.Nature, 408 6815
M. Folstein, M. Folstein, S. Folstein, S. Folstein, P. McHugh, P. McHugh (1975)
“Mini-mental state”: A practical method for grading the cognitive state of patients for the clinicianJournal of Psychiatric Research, 12
D. Selkoe (1997)
Alzheimer's Disease--Genotypes, Phenotype, and TreatmentsScience, 275
J. Hardy, G. Higgins (1992)
Alzheimer's disease: the amyloid cascade hypothesis.Science, 256 5054
S. Pimplikar (2009)
Reassessing the amyloid cascade hypothesis of Alzheimer's disease.The international journal of biochemistry & cell biology, 41 6
L. Mucke, E. Masliah, Gui-qiu Yu, M. Mallory, E. Rockenstein, G. Tatsuno, K. Hu, D. Kholodenko, K. Johnson-wood, L. McConlogue (2000)
High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque FormationThe Journal of Neuroscience, 20
M. Lambert, A. Barlow, B. Chromy, C. Edwards, R. Freed, M. Liosatos, Todd Morgan, I. Rozovsky, B. Trommer, K. Viola, P. Wals, Zhang Chi, C. Finch, G. Krafft, W. Klein (1998)
Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins.Proceedings of the National Academy of Sciences of the United States of America, 95 11
V. Shoshan-Barmatz, Nurit Keinan, Salah Abu-hamad, Dalia Tyomkin, Lior Aram (2010)
Apoptosis is regulated by the VDAC1 N-terminal region and by VDAC oligomerization: release of cytochrome c, AIF and Smac/Diablo.Biochimica et biophysica acta, 1797 6-7
I. Ferrer (2009)
Altered mitochondria, energy metabolism, voltage-dependent anion channel, and lipid rafts converge to exhaust neurons in Alzheimer’s diseaseJournal of Bioenergetics and Biomembranes, 41
T. Hope, J. Keene, Kathy Gedling, S. Cooper, C. Fairburn, R. Jacoby (1997)
Behaviour changes in dementia 1: Point of entry data of a prospective studyInternational Journal of Geriatric Psychiatry, 12
Nathan Majewski, V. Nogueira, Prashanth Bhaskar, Platina Coy, Jennifer Skeen, Kathrin Gottlob, N. Chandel, C. Thompson, R. Robey, N. Hay (2004)
Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak.Molecular cell, 16 5
(2008)
Hexokinase-I protection against apoptotic cell death is mediated via interaction with the voltagedependent anion channel-1: mapping the site of binding
J. Pastorino, J. Hoek (2003)
Hexokinase II: the integration of energy metabolism and control of apoptosis.Current medicinal chemistry, 10 16
Douglas Galasko, S. Edland, J. Morris, C. Clark, R. Mohs, E. Koss (1995)
The Consortium to Establish a Registry for Alzheimer's Disease (CERAD).Neurology, 45
J. Pastorino, J. Hoek, N. Shulga (2005)
Activation of glycogen synthase kinase 3beta disrupts the binding of hexokinase II to mitochondria by phosphorylating voltage-dependent anion channel and potentiates chemotherapy-induced cytotoxicity.Cancer research, 65 22
Yuesong Gong, Lei Chang, K. Viola, P. Lacor, M. Lambert, C. Finch, G. Krafft, W. Klein (2003)
Alzheimer's disease-affected brain: Presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory lossProceedings of the National Academy of Sciences of the United States of America, 100
P. Chapman, G. White, Matt Jones, Deirdre Cooper-Blacketer, V. Marshall, M. Irizarry, L. Younkin, M. Good, T. Bliss, B. Hyman, S. Younkin, K. Hsiao (1999)
Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic miceNature Neuroscience, 2
Ana-María Simón, L. Schiapparelli, P. Salazar-Colocho, M. Cuadrado‐Tejedor, Luis Escribano, R. Maturana, J. Rı́o, Alberto Pérez-Mediavilla, D. Frechilla (2009)
Overexpression of wild-type human APP in mice causes cognitive deficits and pathological features unrelated to Aβ levelsNeurobiology of Disease, 33
S. Lesné, M. Koh, L. Kotilinek, R. Kayed, C. Glabe, A. Yang, M. Gallagher, K. Ashe (2006)
A specific amyloid-beta protein assembly in the brain impairs memory.Nature, 440 7082
H. Braak, E. Braak (1998)
Evolution of neuronal changes in the course of Alzheimer's disease.Journal of neural transmission. Supplementum, 53
M. Sampson, R. Lovell, W. Craigen (1997)
The Murine Voltage-dependent Anion Channel Gene FamilyThe Journal of Biological Chemistry, 272
Hilal Zaid, Salah Abu-hamad, A. Israelson, I. Nathan, V. Shoshan-Barmatz (2005)
The voltage-dependent anion channel-1 modulates apoptotic cell deathCell Death and Differentiation, 12
T. Kawarabayashi, L. Younkin, T. Saido, M. Shoji, K. Ashe, S. Younkin (2001)
Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience, 21 2
(2009)
The pathology of APP transgenic mice: a model of Alzheimer’s disease or sim- M. Cuadrado-Tejedor et al. / VDAC1 in Alzheimer’s Disease 205 ply overexpression of APP
M. Westerman, Deirdre Cooper-Blacketer, A. Mariash, L. Kotilinek, T. Kawarabayashi, L. Younkin, G. Carlson, S. Younkin, K. Ashe (2002)
The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's DiseaseThe Journal of Neuroscience, 22
C. Ramírez, Miriam González, M. Díaz, R. Alonso, I. Ferrer, G. Santpere, B. Puig, G. Meyer, R. Marín (2009)
VDAC and ERα interaction in caveolae from human cortex is altered in Alzheimer's diseaseMolecular and Cellular Neuroscience, 42
G. Mckhann, D. Drachman, M. Folstein, R. Katzman, D. Price, E. Stadlan (2011)
Clinical diagnosis of Alzheimer's disease: Report of the NINCDS—ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's DiseaseNeurology, 77
L. Devi, B. Prabhu, D. Galati, N. Avadhani, H. Anandatheerthavarada (2006)
Accumulation of Amyloid Precursor Protein in the Mitochondrial Import Channels of Human Alzheimer’s Disease Brain Is Associated with Mitochondrial DysfunctionThe Journal of Neuroscience, 26
Xinglong Wang, B. Su, Hyoung-Gon Lee, Xinyi Li, George Perry, Mark Smith, Xiongwei Zhu (2009)
Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer's DiseaseThe Journal of Neuroscience, 29
Tanay Ghosh, N. Pandey, A. Maitra, S. Brahmachari, B. Pillai (2007)
A Role for Voltage-Dependent Anion Channel Vdac1 in Polyglutamine-Mediated Neuronal Cell DeathPLoS ONE, 2
D. Morgan, D. Diamond, P. Gottschall, K. Ugen, C. Dickey, J. Hardy, K. Duff, P. Jantzen, G. Dicarlo, D. Wilcock, K. Connor, J. Hatcher, C. Hope, M. Gordon, G. Arendash (2000)
Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's diseaseNature, 408
(2002)
A[beta] toxicity in Alzheimer’s disease: globular oligomers (ADDLs) as new vaccine and drug targets
E. Pérez-Gracia, B. Torrejón-Escribano, I. Ferrer (2008)
Dystrophic neurites of senile plaques in Alzheimer’s disease are deficient in cytochrome c oxidaseActa Neuropathologica, 116
K. Hsiao, P. Chapman, S. Nilsen, C. Eckman, Y. Harigaya, S. Younkin, Fusheng Yang, G. Cole (1996)
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic MiceScience, 274
J. Biedler, S. Roffler-Tarlov, M. Schachner, L. Freedman (1978)
Multiple neurotransmitter synthesis by human neuroblastoma cell lines and clones.Cancer research, 38 11 Pt 1
M. Roth, E. Tym, C. Mountjoy, F. Huppert, H. Hendrie, S. Verma, R. Goddard (1986)
CAMDEX: A Standardised Instrument for the Diagnosis of Mental Disorder in the Elderly with Special Reference to the Early Detection of DementiaBritish Journal of Psychiatry, 149
D. Selkoe (1999)
Translating cell biology into therapeutic advances in Alzheimer's diseaseNature, 399
D. Selkoe (1997)
Alzheimer's disease: genotypes, phenotypes, and treatments.Science, 275 5300
V. Shoshan-Barmatz, Nurit Keinan, H. Zaid (2008)
Uncovering the role of VDAC in the regulation of cell life and deathJournal of Bioenergetics and Biomembranes, 40
J. Hardy, D. Selkoe (2009)
The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics
T. Kawarabayashi, L. Younkin, T. Saido, M. Shoji, K. Ashe, S. Younkin (2001)
Age-Dependent Changes in Brain, CSF, and Plasma Amyloid β Protein in the Tg2576 Transgenic Mouse Model of Alzheimer's DiseaseThe Journal of Neuroscience, 21
The mitochondrial voltage-dependent anion channel 1 (VDAC1) is involved in the release of apoptotic proteins with possible relevance in Alzheimer's disease (AD) neuropathology. Through proteomic analysis followed by Western blotting and immunohistochemical techniques, we have found that VDAC1 is overexpressed in the hippocampus from amyloidogenic AD transgenic mice models. VDAC1 was also overexpressed in postmortem brain tissue from AD patients at an advanced stage of the disease. Interestingly, amyloid-β (Aβ) soluble oligomers were able to induce upregulation of VDAC1 in a human neuroblastoma cell line, further supporting a correlation between Aβ levels and VDAC1 expression. In hippocampal extracts from transgenic mice, a significant increase was observed in the levels of VDAC1 phosphorylated at an epitope that is susceptible to phosphorylation by glycogen synthase kinase-3β, whose activity was also increased. The levels of hexokinase I (HXKI), which interacts with VDAC1 and affects its function, were decreased in mitochondrial samples from AD models. Since phospho-VDAC and reduced HXKI levels favors a VDAC1 conformational state more prone to the release proapoptotic factors, regulation of the function of this channel may be a promising therapeutic approach to combat AD.
Journal of Alzheimer's Disease – IOS Press
Published: Jan 1, 2011
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