Quantitative MRI reveals aging‐associated T2 changes in mouse models of Alzheimer's disease
暂无分享,去创建一个
M. F. Falangola | Sang-Pil Lee | J. Helpern | J. Babb | A. Bogart | Sangpil Lee | R. Nixon | K. Duff | V. Dyakin | M. F. Falangola | V. V. Dyakin | S. P. Lee | A. Bogart | J. S. Babb | K. Duff | R. Nixon | J. A. Helpern | S. Lee
[1] J. McCarthy,et al. Involvement of presenilins in cell-survival signalling pathways. , 2005, Biochemical Society transactions.
[2] D. Dickson,et al. Amyloid Phenotype Characterization of Transgenic Mice Overexpressing both Mutant Amyloid Precursor Protein and Mutant Presenilin 1 Transgenes , 1999, Neurobiology of Disease.
[3] M. Bunsey,et al. Differential Effects of Dorsal and Ventral Hippocampal Lesions , 1998, The Journal of Neuroscience.
[4] Thomas Wisniewski,et al. Detection of Alzheimer's amyloid in transgenic mice using magnetic resonance microimaging , 2003, Magnetic resonance in medicine.
[5] L. Mucke,et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.
[6] A Van der Linden,et al. Noninvasive in vivo MRI detection of neuritic plaques associated with iron in APP[V717I] transgenic mice, a model for Alzheimer's disease , 2005, Magnetic resonance in medicine.
[7] R. Kauppinen,et al. Graded Reduction of Cerebral Blood Flow in Rat as Detected by the Nuclear Magnetic Resonance Relaxation Time T2: A Theoretical and Experimental Approach , 2000, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[8] Thomas Wisniewski,et al. Amyloid‐β Deposition Is Associated with Decreased Hippocampal Glucose Metabolism and Spatial Memory Impairment in APP/PS1 Mice , 2004 .
[9] D J Jenden,et al. In vivo proton magnetic resonance spectroscopy of the normal aging human brain. , 1996, Life sciences.
[10] J. Hardy,et al. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes , 1998, Nature Medicine.
[11] T. Groen,et al. Transgenic mice expressing the human presenilin 1 gene demonstrate enhanced hippocampal reorganization following entorhinal cortex lesions , 2002, Brain Research Bulletin.
[12] Thomas Wisniewski,et al. Molecular Targeting of Alzheimer's Amyloid Plaques for Contrast-Enhanced Magnetic Resonance Imaging , 2002, Neurobiology of Disease.
[13] Jaime Grutzendler,et al. Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches , 2004, Nature Neuroscience.
[14] Thomas Wisniewski,et al. Magnetic Resonance in Medicine 51:794–798 (2004) MRI Assessment of Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease , 2022 .
[15] B. Hyman,et al. Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss. , 2000, The American journal of pathology.
[16] Joseph A. Helpern,et al. Histological Co-Localization of Iron in Aß Plaques of PS/APP Transgenic Mice , 2005, Neurochemical Research.
[17] M. F. Falangola,et al. Visualization of β‐amyloid plaques in a transgenic mouse model of Alzheimer's disease using MR microscopy without contrast reagents , 2004, Magnetic resonance in medicine.
[18] D. Treit,et al. Dorsal and ventral hippocampal cholinergic systems modulate anxiety in the plus-maze and shock-probe tests , 2002, Brain Research.
[19] Marc Dhenain,et al. Age-related evolution of amyloid burden, iron load, and MR relaxation times in a transgenic mouse model of Alzheimer's disease , 2006, Neurobiology of Disease.
[20] D. Davies,et al. Neurodegenerative Changes Associated with β-Amyloid Deposition in the Brains of Mice Carrying Mutant Amyloid Precursor Protein and Mutant Presenilin-1 Transgenes , 2001, Experimental Neurology.
[21] E. Kandel,et al. Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration , 2004, Neuron.
[22] Clifford R Jack,et al. In Vivo Magnetic Resonance Microimaging of Individual Amyloid Plaques in Alzheimer's Transgenic Mice , 2005, The Journal of Neuroscience.
[23] Susumu Mori,et al. Detection of amyloid plaques in mouse models of Alzheimer's disease by magnetic resonance imaging , 2004, Magnetic resonance in medicine.
[24] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[25] K. Duff,et al. Reorganization of Cholinergic Terminals in the Cerebral Cortex and Hippocampus in Transgenic Mice Carrying Mutated Presenilin-1 and Amyloid Precursor Protein Transgenes , 1999, The Journal of Neuroscience.
[26] Michael Garwood,et al. In vivo visualization of Alzheimer's amyloid plaques by magnetic resonance imaging in transgenic mice without a contrast agent , 2004, Magnetic resonance in medicine.
[27] R. Kesner,et al. Patterns of hippocampal cell loss based on subregional lesions of the hippocampus , 2005, Brain Research.
[28] G. Higgins,et al. Transgenic mouse models of Alzheimer's disease: phenotype and application , 2003, Behavioural pharmacology.
[29] R. Empson,et al. Functional Phenotype in Transgenic Mice Expressing Mutant Human Presenilin-1 , 2000, Neurobiology of Disease.
[30] C. Lemere,et al. Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease. , 2001, The American journal of pathology.
[31] K. Duff,et al. Quantitative histological analysis of amyloid deposition in Alzheimer’s double transgenic mouse brain , 2000, Neuroscience.
[32] J. Hardy,et al. Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.