Liraglutide can reverse memory impairment, synaptic loss and reduce plaque load in aged APP/PS1 mice, a model of Alzheimer's disease

[1]  H. Ruetten,et al.  Cardioprotective effects of lixisenatide in rat myocardial ischemia-reperfusion injury studies , 2013, Journal of Translational Medicine.

[2]  J. Schneider,et al.  Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. , 2012, The Journal of clinical investigation.

[3]  D. Munoz,et al.  An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers. , 2012, The Journal of clinical investigation.

[4]  C. Hölscher,et al.  Drugs developed to treat diabetes, liraglutide and lixisenatide, cross the blood brain barrier and enhance neurogenesis , 2012, BMC Neuroscience.

[5]  C. Hölscher,et al.  Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice , 2012, Neurobiology of Aging.

[6]  S. Kanba,et al.  Glucose tolerance status and risk of dementia in the community , 2011, Neurology.

[7]  Christian Hölscher,et al.  Diabetes as a risk factor for Alzheimer's disease: insulin signalling impairment in the brain as an alternative model of Alzheimer's disease. , 2011, Biochemical Society transactions.

[8]  Christian Hölscher,et al.  The Diabetes Drug Liraglutide Prevents Degenerative Processes in a Mouse Model of Alzheimer's Disease , 2011, The Journal of Neuroscience.

[9]  S. Minoshima,et al.  Insulin resistance and Alzheimer-like reductions in regional cerebral glucose metabolism for cognitively normal adults with prediabetes or early type 2 diabetes. , 2011, Archives of neurology.

[10]  C. Hölscher,et al.  Synaptic Plasticity in the Hippocampus of a APP/PS1 Mouse Model of Alzheimer's Disease Is Impaired in Old but Not Young Mice , 2010, PloS one.

[11]  Talib F. Abbas,et al.  Impairment of synaptic plasticity and memory formation in GLP-1 receptor KO mice: Interaction between type 2 diabetes and Alzheimer's disease , 2009, Behavioural Brain Research.

[12]  F. Müller,et al.  Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease , 2009, Proceedings of the National Academy of Sciences.

[13]  D. Drucker,et al.  Incretin-based therapies for type 2 diabetes mellitus , 2009, Nature Reviews Endocrinology.

[14]  W. Klein,et al.  Insulin Receptor Dysfunction Impairs Cellular Clearance of Neurotoxic Oligomeric Aβ* , 2009, The Journal of Biological Chemistry.

[15]  W. Klein,et al.  Protection of synapses against Alzheimer's-linked toxins: Insulin signaling prevents the pathogenic binding of Aβ oligomers , 2009, Proceedings of the National Academy of Sciences.

[16]  B. Shen,et al.  Seizures induced by GABAB-receptor blockade in early-life induced long-term GABAB receptor hypofunction and kindling facilitation , 2008, Epilepsy Research.

[17]  C. Johanson,et al.  Apolipoprotein E, Amyloid-&bgr;, and Blood-Brain Barrier Permeability in Alzheimer Disease , 2008, Journal of neuropathology and experimental neurology.

[18]  C. Duarte,et al.  Role of the brain‐derived neurotrophic factor at glutamatergic synapses , 2008, British journal of pharmacology.

[19]  W. Klein,et al.  Amyloid beta oligomers induce impairment of neuronal insulin receptors , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[20]  W. Klein,et al.  Aβ Oligomers Induce Neuronal Oxidative Stress through an N-Methyl-D-aspartate Receptor-dependent Mechanism That Is Blocked by the Alzheimer Drug Memantine* , 2007, Journal of Biological Chemistry.

[21]  Suzanne Craft,et al.  Insulin resistance and Alzheimer's disease pathogenesis: potential mechanisms and implications for treatment. , 2007, Current Alzheimer research.

[22]  R. Deane,et al.  Role of the blood-brain barrier in the pathogenesis of Alzheimer's disease. , 2007, Current Alzheimer research.

[23]  N. Greig,et al.  Evidence of GLP-1-mediated neuroprotection in an animal model of pyridoxine-induced peripheral sensory neuropathy , 2007, Experimental Neurology.

[24]  W. Klein,et al.  Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease , 2007, The Journal of Neuroscience.

[25]  D. Wilcock,et al.  Quantification of cerebral amyloid angiopathy and parenchymal amyloid plaques with Congo red histochemical stain , 2006, Nature Protocols.

[26]  Hartwig Wolburg,et al.  Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology , 2006, EMBO reports.

[27]  M. Folstein,et al.  Insulin, insulin-degrading enzyme and amyloid-β peptide in Alzheimer's disease: review and hypothesis , 2006, Neurobiology of Aging.

[28]  K. Jin,et al.  Neurodegeneration and neurogenesis: focus on Alzheimer's disease. , 2006, Current Alzheimer research.

[29]  C. Eckman,et al.  Aβ-degrading enzymes: modulators of Alzheimer's disease pathogenesis and targets for therapeutic intervention , 2005 .

[30]  C. Finch,et al.  Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers , 2004, The Journal of Neuroscience.

[31]  S. Hoyer Glucose metabolism and insulin receptor signal transduction in Alzheimer disease. , 2004, European journal of pharmacology.

[32]  D. Alkon,et al.  Insulin and the insulin receptor in experimental models of learning and memory. , 2004, European journal of pharmacology.

[33]  W. Banks,et al.  Glucagon-like peptide-1 receptor is involved in learning and neuroprotection , 2003, Nature Medicine.

[34]  M. Mattson,et al.  Glucagon‐like peptide‐1 decreases endogenous amyloid‐β peptide (Aβ) levels and protects hippocampal neurons from death induced by Aβ and iron , 2003 .

[35]  D. Selkoe Alzheimer's Disease Is a Synaptic Failure , 2002, Science.

[36]  P. Greengard,et al.  Does insulin dysfunction play a role in Alzheimer's disease? , 2002, Trends in pharmacological sciences.

[37]  Jan Born,et al.  Sniffing neuropeptides: a transnasal approach to the human brain , 2002, Nature Neuroscience.

[38]  T. Bliss,et al.  Brain-Derived Neurotrophic Factor Induces Long-Term Potentiation in Intact Adult Hippocampus: Requirement for ERK Activation Coupled to CREB and Upregulation of Arc Synthesis , 2002, The Journal of Neuroscience.

[39]  W. Pan,et al.  Interactions of glucagon-like peptide-1 (GLP-1) with the blood-brain barrier , 2002, Journal of Molecular Neuroscience.

[40]  M. Staufenbiel,et al.  Amyloid-Associated Neuron Loss and Gliogenesis in the Neocortex of Amyloid Precursor Protein Transgenic Mice , 2002, The Journal of Neuroscience.

[41]  D. Selkoe Clearing the Brain's Amyloid Cobwebs , 2001, Neuron.

[42]  R. D'Hooge,et al.  Applications of the Morris water maze in the study of learning and memory , 2001, Brain Research Reviews.

[43]  G. Collingridge,et al.  Age-Related Impairment of Synaptic Transmission But Normal Long-Term Potentiation in Transgenic Mice that Overexpress the Human APP695SWE Mutant Form of Amyloid Precursor Protein , 2001, The Journal of Neuroscience.

[44]  T. Saido,et al.  Metabolic Regulation of Brain Aβ by Neprilysin , 2001, Science.

[45]  Richard Weindruch,et al.  Gene-expression profile of the ageing brain in mice , 2000, Nature Genetics.

[46]  J. Born,et al.  Central nervous system effects of intranasally administered insulin during euglycemia in men. , 1999, Diabetes.

[47]  F. Maxfield,et al.  Slow Degradation of Aggregates of the Alzheimer’s Disease Amyloid β-Protein by Microglial Cells* , 1997, The Journal of Biological Chemistry.

[48]  J. Chad,et al.  Synaptic release rather than failure in the conditioning pulse results in paired-pulse facilitation during minimal synaptic stimulation in the rat hippocampal CA1 neurones , 1996, Neuroscience Letters.

[49]  D. Johnston,et al.  Using paired-pulse facilitation to probe the mechanisms for long-term potentiation (LTP) , 1995, Journal of Physiology-Paris.

[50]  Scott E. Fraser,et al.  Effects of brain-derived neurotrophic factor on optic axon branching and remodelling in vivo , 1995, Nature.

[51]  C. Hölscher Development of Beta-Amyloid-induced Neurodegeneration in Alzheimer's Disease and Novel Neuroprotective Strategies , 2005, Reviews in the neurosciences.

[52]  N. Greig,et al.  The glucagon-like peptides: a new genre in therapeutic targets for intervention in Alzheimer's disease. , 2002, Journal of Alzheimer's disease : JAD.