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  1. Blood phosphorylated tau elevation as a biomarker in immunoglobulin light chain and transthyretin amyloidosis
  2. Neurofilament light chain may serve as a cross-species blood biomarker to assess aging and predict mortality
  3. Comparative neurofilament light chain trajectories in CSF and plasma in autosomal dominant Alzheimer’s disease
  4. Experimental evidence for temporal uncoupling of brain Aβ deposition and neurodegenerative sequelae
  5. High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer’s Disease-Causing Mutations
  6. Signatures of glial activity can be detected in the CSF proteome
  7. CSF p-tau increase in response to Aβ-type and Danish-type cerebral amyloidosis and in the absence of neurofibrillary tangles
  8. Cerebrospinal fluid cytokine levels are associated with macrophage infiltration into tumor tissues of glioma patients
  9. A neuronal blood marker is associated with mortality in old age
  10. Acute targeting of pre-amyloid seeds in transgenic mice reduces Alzheimer-like pathology later in life
  11. Loss of function of the mitochondrial peptidase PITRM1 induces proteotoxic stress and Alzheimer’s disease-like pathology in human cerebral organoids
  12. Neurofilaments in spinocerebellar ataxia type 3: blood biomarkers at the preataxic and ataxic stage in humans and mice
  13. Loss of function of the mitochondrial peptidase PITRM1 induces proteotoxic stress and Alzheimer’s disease-like pathology in human cerebral organoids
  14. Neurofilaments as blood biomarkers at the preataxic and ataxic stage of spinocerebellar ataxia type 3: a cross-species analysis in humans and mice
  15. Early Aβ reduction prevents progression of cerebral amyloid angiopathy
  16. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease
  17. Amyloid polymorphisms constitute distinct clouds of conformational variants in different etiological subtypes of Alzheimer’s disease
  18. Aβ seeding potency peaks in the early stages of cerebral β‐amyloidosis
  19. Prevention of tau increase in cerebrospinal fluid of APP transgenic mice suggests downstream effect of BACE1 inhibition
  20. Neurofilament Light Chain in Blood and CSF as Marker of Disease Progression in Mouse Models and in Neurodegenerative Diseases
  21. Neurofilament Light Chain in Blood and CSF as Marker of Disease Progression in Mouse Models and in Neurodegenerative Diseases
  22. Conversion of Synthetic Aβ toIn VivoActive Seeds and Amyloid Plaque Formation in a Hippocampal Slice Culture Model
  23. Serum Levels of Progranulin Do Not Reflect Cerebrospinal Fluid Levels in Neurodegenerative Disease
  24. Parenchymal cystatin C focal deposits and glial scar formation around brain arteries in Hereditary Cystatin C Amyloid Angiopathy
  25. Persistence of Aβ seeds in APP null mouse brain
  26. Increased CSF Aβ during the very early phase of cerebral Aβ deposition in mouse models
  27. Highly potent soluble amyloid-β seeds in human Alzheimer brain but not cerebrospinal fluid
  28. Deposition of collagen IV and aggrecan in leptomeningeal arteries of hereditary brain haemorrhage with amyloidosis
  29. Seeded strain‐like transmission of β‐amyloid morphotypes in APP transgenic mice
  30. Changes in Amyloid-β and Tau in the Cerebrospinal Fluid of Transgenic Mice Overexpressing Amyloid Precursor Protein
  31. CSF biomarker variability in the Alzheimer's Association quality control program
  32. BRI2 Protein Regulates β-Amyloid Degradation by Increasing Levels of Secreted Insulin-degrading Enzyme (IDE)
  33. The Alzheimer's Association external quality control program for cerebrospinal fluid biomarkers
  34. Peripherally Applied Aβ-Containing Inoculates Induce Cerebral β-Amyloidosis
  35. Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's disease
  36. Formation and maintenance of Alzheimer's disease β-amyloid plaques in the absence of microglia
  37. Cystatin C modulates cerebral β-amyloidosis
  38. Exogenous Induction of Cerebral ß-Amyloidogenesis Is Governed by Agent and Host
  39. Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
  40. Neocortical synaptic bouton number is maintained despite robust amyloid deposition in APP23 transgenic mice
  41. Extracellular amyloid formation and associated pathology in neural grafts