Amyloid phenotype characterization of transgenic mice overexpressing both mutant amyloid precursor protein and mutant presenilin 1 transgenes.
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Summary
Highly congophilic deposits consisting of N-terminal normal and modified forms of Abeta were identified, reminiscent of those found in human AD brain, and immunohistochemistry and mass spectrometry showed that Abeta42 forms were underrepresented relative to Abeta40, and Abeta43 was undetectable.
- Type
- article
- Published
- 1999-08-01
- Cited by
- 200
- References
- 21
- Access
- Open access
- OpenAlex
- https://openalex.org/W1987686583
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:25442205
Keywords
Presenilin, Gliosis, Genetically modified mouse, Glial fibrillary acidic protein, Transgene
References
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- Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology.
- Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
- Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1
- Amino- and carboxyl-terminal heterogeneity of beta-amyloid peptides deposited in human brain.
- Short- and long-term consequences of intracranial injections of the excitotoxin, quinolinic acid, as evidenced by GFA immunohistochemistry of astrocytes.
- Transection of the rat olfactory nerve increases glial fibrillary acidic protein immunoreactivity from the olfactory bulb to the piriform cortex
- Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins.
- Dominant and differential deposition of distinct beta-amyloid peptide species, A beta N3(pE), in senile plaques.
- The carboxy terminus of the beta amyloid protein is critical for the seeding of amyloid formation: implications for the pathogenesis of Alzheimer's disease.
- Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes
- Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice
- The profile of soluble amyloid beta protein in cultured cell media. Detection and quantification of amyloid beta protein and variants by immunoprecipitation-mass spectrometry.
- Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo
- Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease
- Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Cited by
- Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls.
- Immunomodulation Targeting Abnormal Protein Conformation Reduces Pathology in a Mouse Model of Alzheimer's Disease
- Modulation of Alzheimer’s Pathology in Transgenic Mouse Models
- The pathology of APP transgenic mice: a model of Alzheimer's disease or simply overexpression of APP?
- Efecto del resveratrol en modelos murinos de envejecimiento y enfermedad de Alzheimer
- Postmortale Diagnosestellung bei Morbus Alzheimer
- Transgenic mouse models of Alzheimer's disease: phenotype and application
- [Experimental models in Alzheimer's disease].
- Brain aging in dogs: parallels with human brain aging and Alzheimer's disease.
- Imaging Aβ Plaques in Living Transgenic Mice with Multiphoton Microscopy and Methoxy‐X04, a Systemically Administered Congo Red Derivative
- Evaluation and validation of new animal and behavioural models for the study of Alzheimer's disease
- Die Amyloidablagerung in einem Mausmodell der Alzheimer Demenz und die Modulation der β-Amyloid-Peptidentstehung durch membranverankerte Inhibitoren
- Biological transgenic mouse models of Alzheimer's disease.
- Presenilin‐1 but not amyloid precursor protein mutations present in mouse models of Alzheimer’s disease attenuate the response of cultured cells to γ‐secretase modulators regardless of their potency and structure
- Neurotoxic Aβ peptides increase oxidative stress in vivo through NMDA‐receptor and nitric‐oxide‐synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro
- Effects of Increased Iron Intake During the Neonatal Period on the Brain of Adult AβPP/PS1 Transgenic Mice
- NITRATION AND INACTIVATION OF MANGANESE SUPEROXIDE DISMUTASE PLAYS A CRITICAL ROLE IN METABOLIC SWITCH
- Synthesis, characterization, and preclinical validation of a PET radiopharmaceutical for interrogating Aβ (β-amyloid) plaques in Alzheimer’s disease
- Studies on the first described Alzheimer's disease amyloid β mutant, the Dutch variant
- Identification of a BACE dimer and characterization of its biochemical and enzymatic properties
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