All Stories

  1. Blood plasma biomarkers for Alzheimer’s disease: Aβ1–42/1–40 vs. AβX–42/X–40
  2. Emerging roles of N- and C-terminally truncated Aβ species in Alzheimer’s disease
  3. N-Terminal Truncated Aβ4-42 Is a Substrate for Neprilysin Degradation in vitro and in vivo
  4. Physical Activity Ameliorates Impaired Hippocampal Neurogenesis in the Tg4-42 Mouse Model of Alzheimer’s Disease
  5. 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
  6. The metalloprotease ADAMTS4 generates N-truncated Aβ4–x species and marks oligodendrocytes as a source of amyloidogenic peptides in Alzheimer’s disease
  7. Glycoprotein NMB: a novel Alzheimer’s disease associated marker expressed in a subset of activated microglia
  8. The presubiculum is preserved from neurodegenerative changes in Alzheimer’s disease
  9. Synergistic Effect on Neurodegeneration by N-Truncated Aβ4−42 and Pyroglutamate Aβ3−42 in a Mouse Model of Alzheimer's Disease
  10. N-truncated Aβ4–x peptides in sporadic Alzheimer’s disease cases and transgenic Alzheimer mouse models
  11. Altered neurogenesis in mouse models of Alzheimer disease
  12. Extraction of Soluble and Insoluble Protein Fractions from Mouse Brains and Spinal Cords
  13. Preparation of Crude Synaptosomal Fractions from Mouse Brains and Spinal Cords
  14. Effects of Long-Term Environmental Enrichment on Anxiety, Memory, Hippocampal Plasticity and Overall Brain Gene Expression in C57BL6 Mice
  15. Physical activity delays hippocampal neurodegeneration and rescues memory deficits in an Alzheimer disease mouse model
  16. Deposition of C-terminally truncated Aβ species Aβ37 and Aβ39 in Alzheimer’s disease and transgenic mouse models
  17. The Cannabinoid CB1/CB2 Agonist WIN55212.2 Promotes Oligodendrocyte DifferentiationIn Vitroand Neuroprotection During the Cuprizone-Induced Central Nervous System Demyelination
  18. Endogenous Apolipoprotein E (ApoE) Fragmentation Is Linked to Amyloid Pathology in Transgenic Mouse Models of Alzheimer’s Disease
  19. Alzheimer’s Disease
  20. Immunotherapy Against N-Truncated Amyloid-β Oligomers
  21. Gene Expression Profiling in the APP/PS1KI Mouse Model of Familial Alzheimer’s Disease
  22. N-Truncated Aβ2-X Starting with Position Two in Sporadic Alzheimer’s Disease Cases and Two Alzheimer Mouse Models
  23. Gene Dosage Dependent Aggravation of the Neurological Phenotype in the 5XFAD Mouse Model of Alzheimer's Disease
  24. Neprilysin Deficiency Alters the Neuropathological and Behavioral Phenotype in the 5XFAD Mouse Model of Alzheimer's Disease
  25. I716F AβPP Mutation Associates with the Deposition of Oligomeric Pyroglutamate Amyloid-β and α-Synucleinopathy with Lewy Bodies
  26. Immunocytochemical Detection of Intraneuronal Aβ Peptides in Mouse Models of Alzheimer’s Disease
  27. Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation
  28. Focusing the amyloid cascade hypothesis on N-truncated Abeta peptides as drug targets against Alzheimer’s disease
  29. Deciphering the Molecular Profile of Plaques, Memory Decline and Neuron Loss in Two Mouse Models for Alzheimer’s Disease by Deep Sequencing
  30. Aβ38 in the Brains of Patients with Sporadic and Familial Alzheimer's Disease and Transgenic Mouse Models
  31. Immunolesion-induced loss of cholinergic projection neurones promotes β-amyloidosis and tau hyperphosphorylation in the hippocampus of triple-transgenic mice
  32. Abundance of Aβ5-x like immunoreactivity in transgenic 5XFAD, APP/PS1KI and 3xTG mice, sporadic and familial Alzheimer’s disease
  33. Accelerated tau pathology with synaptic and neuronal loss in a novel triple transgenic mouse model of Alzheimer's disease
  34. Oligomeric Pyroglutamate Amyloid-β is Present in Microglia and a Subfraction of Vessels in Patients with Alzheimer's Disease: Implications for Immunotherapy
  35. N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits
  36. Abundant pyroglutamate-modified ABri and ADan peptides in extracellular and vascular amyloid deposits in familial British and Danish dementias
  37. Early intraneuronal accumulation and increased aggregation of phosphorylated Abeta in a mouse model of Alzheimer’s disease
  38. N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody
  39. Problems During Aging (Alzheimer’s and Others)
  40. The Arctic AβPP mutation leads to Alzheimer’s disease pathology with highly variable topographic deposition of differentially truncated Aβ
  41. Intraneuronal Aβ accumulation and neurodegeneration: Lessons from transgenic models
  42. Amyloid Precursor Protein Is a Biomarker for Transformed Human Pluripotent Stem Cells
  43. No improvement after chronic ibuprofen treatment in the 5XFAD mouse model of Alzheimer's disease
  44. 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
  45. AβPP Accumulation and/or Intraneuronal Amyloid-β Accumulation? The 3xTg-AD Mouse Model Revisited
  46. Pyroglutamate Amyloid β (Aβ) Aggravates Behavioral Deficits in Transgenic Amyloid Mouse Model for Alzheimer Disease
  47. Environmental enrichment fails to rescue working memory deficits, neuron loss, and neurogenesis in APP/PS1KI mice
  48. Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Aβ aggregation in the 5XFAD mouse model of Alzheimer's disease
  49. Pyroglutamate Amyloid-β (Aβ): A Hatchet Man in Alzheimer Disease
  50. Reduced levels of IgM autoantibodies against N-truncated pyroglutamate Aβ in plasma of patients with Alzheimer's disease
  51. Intraneuronal Aβ as a trigger for neuron loss: can this be translated into human pathology?
  52. 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
  53. Identification of Low Molecular Weight Pyroglutamate Aβ Oligomers in Alzheimer Disease
  54. 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
  55. Intracellular Aβ triggers neuron loss in the cholinergic system of the APP/PS1KI mouse model of Alzheimer's disease
  56. Inflammatory changes are tightly associated with neurodegeneration in the brain and spinal cord of the APP/PS1KI mouse model of Alzheimer's disease
  57. Gene expression of neuregulin-1 isoforms in different brain regions of elderly schizophrenia patients
  58. Histone Deacetylase Inhibitor Valproic Acid Inhibits Cancer Cell Proliferation via Down-regulation of the Alzheimer Amyloid Precursor Protein
  59. Intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease
  60. Neuron Loss in Transgenic Mouse Models of Alzheimer's Disease
  61. Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Aβ peptides in mouse models of Alzheimer's disease
  62. Pyroglutamate Abeta pathology in APP/PS1KI mice, sporadic and familial Alzheimer’s disease cases
  63. Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model
  64. Circulating immune complexes of Aβ and IgM in plasma of patients with Alzheimer’s disease
  65. APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy
  66. Die modifizierte Amyloid-Hypothese der Alzheimer-Demenz – intraneuronales Abeta induziert Neurodegeneration
  67. Transient intraneuronal Aβ rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice
  68. Effect of copper intake on CSF parameters in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial
  69. Early Intraneuronal β-Amyloid Pathology: Do Transgenic Mice Represent Valid Model Systems?
  70. Alzheimer-Demenz
  71. Age-dependent loss of dentate gyrus granule cells in APP/PS1KI mice
  72. Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease
  73. Motor impairment in Alzheimer’s disease and transgenic Alzheimer’s disease mouse models
  74. Review on the APP/PS1KI mouse model: intraneuronal Aβ accumulation triggers axonopathy, neuron loss and working memory impairment
  75. Intraneuronal β-Amyloid Is a Major Risk Factor – Novel Evidence from the APP/PS1KI Mouse Model
  76. Age-dependent axonal degeneration in an Alzheimer mouse model
  77. Altered cholesterol metabolism in APP695-transfected neuroblastoma cells
  78. Gender dependent APP processing in a transgenic mouse model of Alzheimer’s disease
  79. Axonopathy in an APP/PS1 transgenic mouse model of Alzheimer’s disease
  80. Decreased plasma cholesterol levels during aging in transgenic mouse models of Alzheimer's disease
  81. OTX1 and OTX2 Expression Correlates With the Clinicopathologic Classification of Medulloblastomas
  82. Traumatic brain injury: cause or risk of Alzheimer’s disease? A review of experimental studies
  83. A modified beta-amyloid hypothesis: intraneuronal accumulation of the beta-amyloid peptide - the first step of a fatal cascade
  84. Time sequence of maturation of dystrophic neurites associated with Aβ deposits in APP/PS1 transgenic mice
  85. No alterations of hippocampal neuronal number and synaptic bouton number in a transgenic mouse model expressing the β-cleaved C-terminal APP fragment
  86. α-Synuclein, Aβ and Alzheimer's disease
  87. Reelin in plaques of β-amyloid precursor protein and presenilin-1 double-transgenic mice
  88. Intraneuronal Aβ accumulation precedes plaque formation in β-amyloid precursor protein and presenilin-1 double-transgenic mice