C. Glabe

发表

Different Conformations of Amyloid β Induce Neurotoxicity by Distinct Mechanisms in Human Cortical Neurons

J. Busciglio, A. Deshpande, E. Mina, 2006, The Journal of Neuroscience.

Intracellular Injection of Brain Extracts from Alzheimer’s Disease Patients Triggers Unregulated Ca2+ Release from Intracellular Stores That Hinders Cellular Bioenergetics

G. Ullah, I. Parker, A. Demuro, 2022, bioRxiv.

NMDA receptor activation inhibits alpha-secretase and promotes neuronal amyloid-beta production.

E. Mackenzie, C. Gabriel, C. Ali, 2005, The Journal of neuroscience : the official journal of the Society for Neuroscience.

Amyloid β -Peptide and Oligomers in the Brain and CSF of Aged Canines

M. Murphy, R. Kayed, E. Head, 2010 .

Intracellular Accumulation of Insoluble, Newly Synthesized Aβn-42 in Amyloid Precursor Protein-transfected Cells That Have Been Treated with Aβ1–42*

A. Yang, A. Henschen, C. Glabe, 1999, The Journal of Biological Chemistry.

Complement activation by cross‐linked truncated and chimeric full‐length β‐amyloid

D. Cribbs, A. Tenner, C. Glabe, 1997, Neuroreport.

G. Brewer, C. Glabe, Joshua McWhirt, 2022, Journal of Alzheimer's disease : JAD.

Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer’s disease

M. Ehrlich, S. Gandy, Minghui Wang, 2022, Alzheimer's & dementia : the journal of the Alzheimer's Association.

A Role for Synaptic Zinc in Activity-Dependent Aβ Oligomer Formation and Accumulation at Excitatory Synapses

R. Metherate, J. Busciglio, A. Deshpande, 2009, The Journal of Neuroscience.

Loss of endosomal/lysosomal membrane impermeability is an early event in amyloid Aβ1‐42 pathogenesis

A. Yang, Lawrence Margol, C. Glabe, 1998, Journal of neuroscience research.

Examination of potential mechanisms of amyloid-induced defects in neuronal transport

Rhiannon L. Nolan, Sameer B. Shah, L. Goldstein, 2009, Neurobiology of Disease.

NMDA Receptor Activation Inhibits α-Secretase and Promotes Neuronal Amyloid-β Production

E. Mackenzie, C. Gabriel, C. Ali, 2005, The Journal of Neuroscience.

Complement Component C1q Modulates the Phagocytosis of Aβ by Microglia

A. Yang, S. Webster, A. Tenner, 2000, Experimental Neurology.

Amyloid β protein is internalized selectively by hippocampal field CA1 and causes neurons to accumulate amyloidogenic carboxyterminal fragments of the amyloid precursor protein

G. Lynch, B. Bahr, A. Yang, 1998 .

Progressive accumulation of amyloid‐β oligomers in Alzheimer’s disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins

J. Yates, D. Salmon, D. Galasko, 2010, The FEBS journal.

Systemic vaccination with anti‐oligomeric monoclonal antibodies improves cognitive function by reducing Aβ deposition and tau pathology in 3xTg‐AD mice

F. LaFerla, Jessica W. Wu, H. Martínez-Coria, 2013, Journal of neurochemistry.

Antibodies against β‐amyloid reduce aβ oligomers, glycogen synthase kinase‐3β activation and τ phosphorylation in vivo and in vitro

B. Teter, S. Frautschy, Surendra S. Ambegaokar, 2006 .

Antibody-Mediated Phagocytosis of the Amyloid β-Peptide in Microglia Is Differentially Modulated by C1q1

S. Webster, E. Ferran, A. Tenner, 2001, The Journal of Immunology.

Soluble fibrillar oligomer levels are elevated in Alzheimer's disease brain and correlate with cognitive dysfunction

C. Glabe, E. Head, Jennifer L. Tomic, 2009, Neurobiology of Disease.

Cultured Rat Microglia Express C1q and Receptor for C1q: Implications for Amyloid Effects on Microglia

C. Cotman, D. Cribbs, A. Tenner, 1995, Experimental Neurology.

NMDAReceptorActivationInhibits-Secretaseand PromotesNeuronalAmyloid-Production

C. Glabe, 2005 .

Proneurogenic Group II mGluR antagonist improves learning and reduces anxiety in Alzheimer Aβ oligomer mouse

M. Ehrlich, C. Barlow, F. Gage, 2014, Molecular Psychiatry.

Latrepirdine improves cognition and arrests progression of neuropathology in an Alzheimer's mouse model

G. Petsko, J. Buxbaum, D. Ringe, 2013, Molecular Psychiatry.

Intracellular accumulation and resistance to degradation of the Alzheimer amyloid A4/beta protein.

C. Glabe, C. Glabe, B. Soreghan, 1992, Proceedings of the National Academy of Sciences of the United States of America.

Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid

C. Cotman, C. Glabe, D. Cribbs, 2008, Journal of Neuroinflammation.

Novel Aβ peptide immunogens modulate plaque pathology and inflammation in a murine model of Alzheimer's disease

R. Kayed, D. Cribbs, M. Fonseca, 2005, Journal of Neuroinflammation.

Single Particle Characterization of Iron-induced Pore-forming

W. Duan, K. Danzer, C. Glabe, 2008 .

Progressive accumulation of amyloid‐β oligomers in Alzheimer’s disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins

J. Yates, D. Salmon, D. Galasko, 2010, The FEBS journal.

Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid

D. Cribbs, C. Glabe, K. Nichol, 2008, Journal of Neuroinflammation.

522 Abnormal homeostasis of pH and zinc: The prelude for cerebral Aβ amyloid formation?

R. Tanzi, A. Bush, C. Atwood, 1996, Neurobiology of Aging.

Novel Aβ peptide immunogens modulate plaque pathology and inflammation in a murine model of Alzheimer's disease

R. Kayed, C. Glabe, D. Cribbs, 2005, Journal of Neuroinflammation.