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Alterations of ATG4A and LC3B in neurons derived from Alzheimer's disease patients.
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- Genes to Cells, 2023, v. 28, n. 4, p. 319, doi. 10.1111/gtc.13010
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- Article
The dopaminergic system promotes neprilysin-mediated degradation of amyloid-β in the brain.
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- Science Signaling, 2024, v. 17, n. 848, p. 1, doi. 10.1126/scisignal.adk1822
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- Article
In Vivo Positron Emission Tomographic Imaging of Glial Responses to Amyloid-β and Tau Pathologies in Mouse Models of Alzheimer's Disease and Related Disorders.
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- Journal of Neuroscience, 2011, v. 31, n. 12, p. 4720, doi. 10.1523/JNEUROSCI.3076-10.2011
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- Article
Cleavage of the Vesicular GABA Transporter under Excitotoxic Conditions Is Followed by Accumulation of the Truncated Transporter in Nonsynaptic Sites.
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- Journal of Neuroscience, 2011, v. 31, n. 12, p. 4622, doi. 10.1523/JNEUROSCI.3541-10.2011
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- Article
Longitudinal, Quantitative Assessment of Amyloid, Neuroinflammation, and Anti-Amyloid Treatment in a Living Mouse Model of Alzheimer's Disease Enabled by Positron Emission Tomography.
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- Journal of Neuroscience, 2007, v. 27, n. 41, p. 10957, doi. 10.1523/JNEUROSCI.0673-07.2007
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- Article
Activity‐dependent cleavage of dyskinesia‐related proline‐rich transmembrane protein 2 (PRRT2) by calpain in mouse primary cortical neurons.
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- FASEB Journal, 2020, v. 34, n. 1, p. 180, doi. 10.1096/fj.201902148R
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- Article
Mechanistic involvement of the calpain-calpastatin system in Alzheimer neuropathology.
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- FASEB Journal, 2012, v. 26, n. 3, p. 1204, doi. 10.1096/fj.11-187740
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An alternative metabolic pathway of amyloid precursor protein C-terminal fragments via cathepsin B in a human neuroglioma model.
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- FASEB Journal, 2011, v. 25, n. 10, p. 3720, doi. 10.1096/fj.11-182154
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- Article
Calpastatin, an endogenous calpain-inhibitor protein, regulates the cleavage of the Cdk5 activator p35 to p25.
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- Journal of Neurochemistry, 2011, v. 117, n. 3, p. 504, doi. 10.1111/j.1471-4159.2011.07222.x
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- Article
The novel β-secretase inhibitor KMI-429 reduces amyloid β peptide production in amyloid precursor protein transgenic and wild-type mice.
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- Journal of Neurochemistry, 2006, v. 96, n. 2, p. 533, doi. 10.1111/j.1471-4159.2005.03576.x
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- Article
Altered expression of neprilysin family members in the pituitary gland of sleep-disturbed rats, an animal model of severe fatigue.
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- Journal of Neurochemistry, 2005, v. 95, n. 4, p. 1156, doi. 10.1111/j.1471-4159.2005.03436.x
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- Article
Nasal vaccine delivery attenuates brain pathology and cognitive impairment in tauopathy model mice.
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- NPJ Vaccines, 2020, v. 5, n. 1, p. 1, doi. 10.1038/s41541-020-0172-y
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- Article
Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells.
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- Scientific Reports, 2019, v. 9, n. 1, p. N.PAG, doi. 10.1038/s41598-019-43535-6
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- Article
A role for calpain-dependent cleavage of TDP-43 in amyotrophic lateral sclerosis pathology.
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- Nature Communications, 2012, v. 3, n. 12, p. 1307, doi. 10.1038/ncomms2303
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- Article
An aberrant sugar modification of BACE1 blocks its lysosomal targeting in Alzheimer's disease.
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- EMBO Molecular Medicine, 2015, v. 7, n. 2, p. 175, doi. 10.15252/emmm.201404438
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- Article
Therapeutic strategies of Alzheimer's disease through manipulation of Aβ metabolism: a focus on Aβ-degrading peptidase, neprilysin.
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- Drug Development Research, 2002, v. 56, n. 2, p. 171, doi. 10.1002/ddr.10073
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- Article
Involvement of calpains in adult neurogenesis: implications for stroke.
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- Frontiers in Cellular Neuroscience, 2015, v. 8/9, p. 1, doi. 10.3389/fncel.2015.00022
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- Article
Proline-rich transmembrane protein 2 knock-in mice present dopamine-dependent motor deficits.
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- Journal of Biochemistry, 2023, v. 174, n. 6, p. 561, doi. 10.1093/jb/mvad074
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- Article
role of TREM2 N-glycans in trafficking to the cell surface and signal transduction of TREM2.
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- Journal of Biochemistry, 2022, v. 172, n. 6, p. 347, doi. 10.1093/jb/mvac073
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- Article
A simplified and sensitive method to identify Alzheimer's disease biomarker candidates using patient-derived induced pluripotent stem cells (iPSCs).
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- Journal of Biochemistry, 2017, v. 162, n. 6, p. 391, doi. 10.1093/jb/mvx058
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- Article
Paradigm shift from diagnosing patients based on common symptoms to categorizing patients into subtypes with different pathogenic mechanisms to guide treatment for Alzheimer's disease.
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- Journal of Biochemistry, 2017, v. 161, n. 6, p. 463, doi. 10.1093/jb/mvx015
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- Article
Biochemical Identification of the Neutral Endopeptidase Family Member Responsible for the Catabolism of Amyloid β Peptide in the Brain1.
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- Journal of Biochemistry, 2000, v. 128, n. 6, p. 897, doi. 10.1093/oxfordjournals.jbchem.a022839
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- Article
Glycosylation regulates degradation of bace1 in lysosome.
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- Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 2014, v. 10, p. P193, doi. 10.1016/j.jalz.2014.04.227
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- Article
Autophagy deficiency increases beta-amyloid pathology and memory impairment in APP transgenic mice
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- 2012
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- Abstract
APP knock-in mouse: A novel and more relevant model mouse for Alzheimer's disease
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- 2012
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Brain endothelial cells produce amyloid-β from amyloid precursor protein 770 and preferentially secrete the O-glycosylated form
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- 2011
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Reactive astrogliosis enhances pyroGlu-Aβ formation via up regulation of glutaminyl cyclase, and reduced neprilysin activity exacerbates this process
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- 2010
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Aβ43 is potently amyloidogenic in vivo
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- 2010
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Deletion of vitamin E increases Aβ accumulation by decreasing its clearances from brain and blood in a mouse model of Alzheimer's disease
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- 2010
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Reduced neprilysin activity is associated with increased formation of pyroglutamylated amyloid-β peptides through upregulation of aminopeptidases and glutaminyl cyclase in brain
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- 2009
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The biological effects of R278I-Presenilin-1 familial mutation on γ-secretase activity and amyloid pathology
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- 2009
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P1-434: Accumulation of Aβ starting with pyroglutamate at position 3 in the brain and its impact on amyloid pathology of Alzheimer's disease
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- 2008
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P1-114: The second generation mouse model for Alzheimer disease
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- 2008
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P1-113: Accecelerated Aβ plaque formation by low level expression of presenilin-1 with R278I mutation in knock-in mouse
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- 2008
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- Abstract
P4-010: Cognitive impairment caused by neprilysin-sensitive Aβ-oligomers in mice
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- 2006
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P1-070: Novel mouse model for Alzheimer’s disease
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- 2006
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P4-010: Cognitive impairment caused by neprilysin-sensitive Aβ-oligomers in mice
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- 2006
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- Abstract
P1-070: Novel mouse model for Alzheimer’s disease
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- 2006
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- Abstract
Amyloid Beta Annular Protofibrils in Cell Processes and Synapses Accumulate with Aging and Alzheimer-Associated Genetic Modification.
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- International Journal of Alzheimer's Disease, 2009, v. 2009, p. 1, doi. 10.4061/2009/689285
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- Article
Anti-Aβ Drug Screening Platform Using Human iPS Cell- Derived Neurons for the Treatment of Alzheimer's Disease.
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- PLoS ONE, 2011, v. 6, n. 9, p. 1, doi. 10.1371/journal.pone.0025788
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Recent Advances in the Modeling of Alzheimer's Disease.
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- Frontiers in Neuroscience, 2022, v. 16, p. 1, doi. 10.3389/fnins.2022.807473
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- Article
Loss of neprilysin alters protein expression in the brain of Alzheimer's disease model mice.
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- Proteomics, 2015, v. 15, n. 19, p. 3349, doi. 10.1002/pmic.201400211
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- Article
The potential role of amyloid in the pathogenesis of age-related macular degeneration.
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- Journal of Clinical Investigation, 2005, v. 115, n. 10, p. 2793, doi. 10.1172/JCI24635
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- Article
Presynaptic Localization of Neprilysin Contributes to Efficient Clearance of Amyloid-β Peptide in Mouse Brain.
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- Journal of Neuroscience, 2004, v. 24, n. 4, p. 991, doi. 10.1523/JNEUROSCI.4792-03.2004
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- Article
Matrix metalloproteinase (MMP) system in brain: identification and characterization of brain-specific MMP highly expressed in cerebellum.
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- European Journal of Neuroscience, 2001, v. 13, n. 5, p. 935, doi. 10.1046/j.0953-816X.2001.01462.x
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Gene therapy in Alzheimer’s disease – potential for disease modification.
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- Journal of Cellular & Molecular Medicine, 2010, v. 14, n. 4, p. 741, doi. 10.1111/j.1582-4934.2010.01038.x
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- Article
Somatostatin regulates brain amyloidßpeptide Aß<sub>42</sub> through modulation of proteolytic degradation.
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- Nature Medicine, 2005, v. 11, n. 4, p. 434, doi. 10.1038/nm1206
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Reply to: 'Clearance of amyloid b-peptide from brain: transport or metabolism?'.
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- Nature Medicine, 2000, v. 6, n. 7, p. 718, doi. 10.1038/77399
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Identification of the major Aβ<sub>1?42</sub>-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition.
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- Nature Medicine, 2000, v. 6, n. 2, p. 143, doi. 10.1038/72237
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Single App knock-in mouse models of Alzheimer's disease.
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- Nature Neuroscience, 2014, v. 17, n. 5, p. 661, doi. 10.1038/nn.3697
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- Article