All Stories

  1. Characterization of a pathogenic gain-of-function mutation in the N-terminal domain of STAT1 which is reported to be associated with eosinophilic esophagitis
  2. Behavioral assessment and gene expression changes in a mouse model with dysfunctional STAT1 signaling
  3. N-terminal truncation of STAT1 transcription factor causes CD3- and CD20-negative non-Hodgkin lymphoma through upregulation of STAT3-mediated oncogenic functions
  4. Cognitive decline and neuroinflammation in a mouse model of obesity: An accelerating role of ageing
  5. Social inhibition in depressed patients is associated with an altered activation profile of the interleukin-6-inducible transcription factor STAT3
  6. Caffeine and potential use in Alzheimer’s disease
  7. Identification of isoAsp7-Aβ as a major Aβ variant in Alzheimer’s disease, dementia with Lewy bodies and vascular dementia
  8. Apolipoprotein E aggregation in microglia initiates Alzheimer’s disease pathology by seeding β-amyloidosis
  9. Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice
  10. Amino‐terminally elongated Aβ peptides are generated by the secreted metalloprotease ADAMTS4 and deposit in a subset of Alzheimer's disease brains
  11. Assessment of immunoprecipitation with subsequent immunoassays for the blood-based diagnosis of Alzheimer’s disease
  12. Blood plasma biomarkers for Alzheimer’s disease: Aβ1–42/1–40 vs. AβX–42/X–40
  13. A novel interface between the N-terminal and coiled-coil domain of STAT1 functions in an auto-inhibitory manner
  14. Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease
  15. Brain Region-Specific Differences in Amyloid-β Plaque Composition in 5XFAD Mice
  16. Lack of STAT1 co-operative DNA binding protects against adverse cardiac remodelling in acute myocardial infarction
  17. Matrix Development for the Detection of Phosphorylated Amyloid-β Peptides by MALDI-TOF-MS
  18. A Combination of Caffeine Supplementation and Enriched Environment in an Alzheimer’s Disease Mouse Model
  19. Is plasma amyloid-β 1–42/1–40 a better biomarker for Alzheimer’s disease than AβX–42/X–40?
  20. Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor
  21. Combined long-term enriched environment and caffeine supplementation improve memory function in C57Bl6 mice
  22. An inhibitory effect on the nuclear accumulation of phospho-STAT1 by its unphosphorylated form
  23. Meprin β knockout reduces brain Aβ levels and rescues learning and memory impairments in the APP/lon mouse model for Alzheimer’s disease
  24. Detection and quantification of Aβ−3–40 (APP669‐711) in cerebrospinal fluid
  25. Long-term caffeine treatment of Alzheimer mouse models ameliorates behavioural deficits and neuron loss and promotes cellular and molecular markers of neurogenesis
  26. Interferon-driven brain phenotype in a mouse model of RNaseT2 deficient leukoencephalopathy
  27. The anti-parallel dimer binding interface in STAT3 transcription factor is required for the inactivation of cytokine-mediated signal transduction
  28. A microRNA signature that correlates with cognition and is a target against cognitive decline
  29. Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau
  30. Evaluation of cerebrospinal fluid glycoprotein NMB (GPNMB) as a potential biomarker for Alzheimer’s disease
  31. Physical activity and cognitive stimulation ameliorate learning and motor deficits in a transgenic mouse model of Alzheimer’s disease
  32. Alzheimer’s Disease
  33. Immunotherapy Targeting Amyloid-ß Peptides in Alzheimer’s Disease
  34. Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models
  35. Chronic Memantine Treatment Ameliorates Behavioral Deficits, Neuron Loss, and Impaired Neurogenesis in a Model of Alzheimer’s Disease
  36. Development and Technical Validation of an Immunoassay for the Detection of APP669–711 (Aβ−3–40) in Biological Samples
  37. N‐terminal heterogeneity of parenchymal and vascular amyloid‐β deposits in Alzheimer’s disease
  38. Loss of Hippocampal Calretinin and Parvalbumin Interneurons in the 5XFAD Mouse Model of Alzheimer’s Disease
  39. Emerging roles of N- and C-terminally truncated Aβ species in Alzheimer’s disease
  40. N-Terminally Truncated Aß Peptide Variants in Alzheimer’s Disease
  41. N-Terminal Truncated Aβ4-42 Is a Substrate for Neprilysin Degradation in vitro and in vivo
  42. Physical Activity Ameliorates Impaired Hippocampal Neurogenesis in the Tg4-42 Mouse Model of Alzheimer’s Disease
  43. A two-step immunoassay for the simultaneous assessment of Aβ38, Aβ40 and Aβ42 in human blood plasma supports the Aβ42/Aβ40 ratio as a promising biomarker candidate of Alzheimer’s disease
  44. The metalloprotease ADAMTS4 generates N-truncated Aβ4–x species and marks oligodendrocytes as a source of amyloidogenic peptides in Alzheimer’s disease
  45. Glycoprotein NMB: a novel Alzheimer’s disease associated marker expressed in a subset of activated microglia
  46. The presubiculum is preserved from neurodegenerative changes in Alzheimer’s disease
  47. Synergistic Effect on Neurodegeneration by N-Truncated Aβ4−42 and Pyroglutamate Aβ3−42 in a Mouse Model of Alzheimer's Disease
  48. N-truncated Aβ4–x peptides in sporadic Alzheimer’s disease cases and transgenic Alzheimer mouse models
  49. Altered neurogenesis in mouse models of Alzheimer disease
  50. Extraction of Soluble and Insoluble Protein Fractions from Mouse Brains and Spinal Cords
  51. Preparation of Crude Synaptosomal Fractions from Mouse Brains and Spinal Cords
  52. Effects of Long-Term Environmental Enrichment on Anxiety, Memory, Hippocampal Plasticity and Overall Brain Gene Expression in C57BL6 Mice
  53. Physical activity delays hippocampal neurodegeneration and rescues memory deficits in an Alzheimer disease mouse model
  54. Deposition of C-terminally truncated Aβ species Aβ37 and Aβ39 in Alzheimer’s disease and transgenic mouse models
  55. The Cannabinoid CB1/CB2 Agonist WIN55212.2 Promotes Oligodendrocyte DifferentiationIn Vitroand Neuroprotection During the Cuprizone-Induced Central Nervous System Demyelination
  56. Endogenous Apolipoprotein E (ApoE) Fragmentation Is Linked to Amyloid Pathology in Transgenic Mouse Models of Alzheimer’s Disease
  57. Alzheimer’s Disease
  58. Immunotherapy Against N-Truncated Amyloid-β Oligomers
  59. Gene Expression Profiling in the APP/PS1KI Mouse Model of Familial Alzheimer’s Disease
  60. N-Truncated Aβ2-X Starting with Position Two in Sporadic Alzheimer’s Disease Cases and Two Alzheimer Mouse Models
  61. Gene Dosage Dependent Aggravation of the Neurological Phenotype in the 5XFAD Mouse Model of Alzheimer's Disease
  62. Neprilysin Deficiency Alters the Neuropathological and Behavioral Phenotype in the 5XFAD Mouse Model of Alzheimer's Disease
  63. I716F AβPP Mutation Associates with the Deposition of Oligomeric Pyroglutamate Amyloid-β and α-Synucleinopathy with Lewy Bodies
  64. Immunocytochemical Detection of Intraneuronal Aβ Peptides in Mouse Models of Alzheimer’s Disease
  65. Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation
  66. Focusing the amyloid cascade hypothesis on N-truncated Abeta peptides as drug targets against Alzheimer’s disease
  67. Deciphering the Molecular Profile of Plaques, Memory Decline and Neuron Loss in Two Mouse Models for Alzheimer’s Disease by Deep Sequencing
  68. Aβ38 in the Brains of Patients with Sporadic and Familial Alzheimer's Disease and Transgenic Mouse Models
  69. Immunolesion-induced loss of cholinergic projection neurones promotes β-amyloidosis and tau hyperphosphorylation in the hippocampus of triple-transgenic mice
  70. Abundance of Aβ5-x like immunoreactivity in transgenic 5XFAD, APP/PS1KI and 3xTG mice, sporadic and familial Alzheimer’s disease
  71. Accelerated tau pathology with synaptic and neuronal loss in a novel triple transgenic mouse model of Alzheimer's disease
  72. Oligomeric Pyroglutamate Amyloid-β is Present in Microglia and a Subfraction of Vessels in Patients with Alzheimer's Disease: Implications for Immunotherapy
  73. N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits
  74. Abundant pyroglutamate-modified ABri and ADan peptides in extracellular and vascular amyloid deposits in familial British and Danish dementias
  75. Early intraneuronal accumulation and increased aggregation of phosphorylated Abeta in a mouse model of Alzheimer’s disease
  76. N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody
  77. Problems During Aging (Alzheimer’s and Others)
  78. The Arctic AβPP mutation leads to Alzheimer’s disease pathology with highly variable topographic deposition of differentially truncated Aβ
  79. Intraneuronal Aβ accumulation and neurodegeneration: Lessons from transgenic models
  80. Amyloid Precursor Protein Is a Biomarker for Transformed Human Pluripotent Stem Cells
  81. No improvement after chronic ibuprofen treatment in the 5XFAD mouse model of Alzheimer's disease
  82. Antibody 9D5 Recognizes Oligomeric Pyroglutamate Amyloid-β in a Fraction of Amyloid-β Deposits in Alzheimer's Disease without Cross-Reactivity with other Protein Aggregates
  83. AβPP Accumulation and/or Intraneuronal Amyloid-β Accumulation? The 3xTg-AD Mouse Model Revisited
  84. Pyroglutamate Amyloid β (Aβ) Aggravates Behavioral Deficits in Transgenic Amyloid Mouse Model for Alzheimer Disease
  85. Environmental enrichment fails to rescue working memory deficits, neuron loss, and neurogenesis in APP/PS1KI mice
  86. Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Aβ aggregation in the 5XFAD mouse model of Alzheimer's disease
  87. Pyroglutamate Amyloid-β (Aβ): A Hatchet Man in Alzheimer Disease
  88. Reduced levels of IgM autoantibodies against N-truncated pyroglutamate Aβ in plasma of patients with Alzheimer's disease
  89. Intraneuronal Aβ as a trigger for neuron loss: can this be translated into human pathology?
  90. Overexpression of Glutaminyl Cyclase, the Enzyme Responsible for Pyroglutamate Aβ Formation, Induces Behavioral Deficits, and Glutaminyl Cyclase Knock-out Rescues the Behavioral Phenotype in 5XFAD Mice
  91. Identification of Low Molecular Weight Pyroglutamate Aβ Oligomers in Alzheimer Disease
  92. Concomitant detection of β-amyloid peptides with N-terminal truncation and different C-terminal endings in cortical plaques from cases with Alzheimer's disease, senile monkeys and triple transgenic mice
  93. Intracellular Aβ triggers neuron loss in the cholinergic system of the APP/PS1KI mouse model of Alzheimer's disease
  94. Inflammatory changes are tightly associated with neurodegeneration in the brain and spinal cord of the APP/PS1KI mouse model of Alzheimer's disease
  95. Accumulation of intraneuronal Aβ correlates with ApoE4 genotype
  96. Gene expression of neuregulin-1 isoforms in different brain regions of elderly schizophrenia patients
  97. Histone Deacetylase Inhibitor Valproic Acid Inhibits Cancer Cell Proliferation via Down-regulation of the Alzheimer Amyloid Precursor Protein
  98. Intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease
  99. Neuron Loss in Transgenic Mouse Models of Alzheimer's Disease
  100. Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Aβ peptides in mouse models of Alzheimer's disease
  101. Pyroglutamate Abeta pathology in APP/PS1KI mice, sporadic and familial Alzheimer’s disease cases
  102. Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model
  103. Circulating immune complexes of Aβ and IgM in plasma of patients with Alzheimer’s disease
  104. APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy
  105. Die modifizierte Amyloid-Hypothese der Alzheimer-Demenz – intraneuronales Abeta induziert Neurodegeneration
  106. Transient intraneuronal Aβ rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice
  107. Effect of copper intake on CSF parameters in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial
  108. Early Intraneuronal β-Amyloid Pathology: Do Transgenic Mice Represent Valid Model Systems?
  109. Alzheimer-Demenz
  110. Age-dependent loss of dentate gyrus granule cells in APP/PS1KI mice
  111. Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease
  112. Motor impairment in Alzheimer’s disease and transgenic Alzheimer’s disease mouse models
  113. Review on the APP/PS1KI mouse model: intraneuronal Aβ accumulation triggers axonopathy, neuron loss and working memory impairment
  114. Intraneuronal β-Amyloid Is a Major Risk Factor – Novel Evidence from the APP/PS1KI Mouse Model
  115. Age-dependent axonal degeneration in an Alzheimer mouse model
  116. Altered cholesterol metabolism in APP695-transfected neuroblastoma cells
  117. Gender dependent APP processing in a transgenic mouse model of Alzheimer’s disease
  118. Axonopathy in an APP/PS1 transgenic mouse model of Alzheimer’s disease
  119. Decreased plasma cholesterol levels during aging in transgenic mouse models of Alzheimer's disease
  120. OTX1 and OTX2 Expression Correlates With the Clinicopathologic Classification of Medulloblastomas
  121. Traumatic brain injury: cause or risk of Alzheimer’s disease? A review of experimental studies
  122. A modified beta-amyloid hypothesis: intraneuronal accumulation of the beta-amyloid peptide - the first step of a fatal cascade
  123. Time sequence of maturation of dystrophic neurites associated with Aβ deposits in APP/PS1 transgenic mice
  124. No alterations of hippocampal neuronal number and synaptic bouton number in a transgenic mouse model expressing the β-cleaved C-terminal APP fragment
  125. α-Synuclein, Aβ and Alzheimer's disease
  126. Reelin in plaques of β-amyloid precursor protein and presenilin-1 double-transgenic mice
  127. Intraneuronal Aβ accumulation precedes plaque formation in β-amyloid precursor protein and presenilin-1 double-transgenic mice