All Stories

  1. GABAergic hyperinnervation of dentate granule cells in the Ts65Dn mouse model of down syndrome: Exploring the role ofApp
  2. Physical exercise induces structural alterations in the hippocampal astrocytes: exploring the role of BDNF-TrkB signaling
  3. Noradrenergic System in Down Syndrome and Alzheimer's Disease A Target for Therapy
  4. Recent Advances in Alzheimer Research
  5. Preface
  6. Concluding Remarks
  7. Further validation to support clinical translation of [18F]FTC-146 for imaging sigma-1 receptors
  8. Increased incidence of intermittent hypoxemia in the Ts65Dn mouse model of Down syndrome
  9. Increased cortical synaptic activation of TrkB and downstream signaling markers in a mouse model of Down Syndrome
  10. Assessment of Dendritic Arborization in the Dentate Gyrus of the Hippocampal Region in Mice
  11. The Link Between Physical Activity and Cognitive Dysfunction in Alzheimer Disease
  12. Nest building is impaired in the Ts65Dn mouse model of Down syndrome and rescued by blocking 5HT2a receptors
  13. The role of NMDA receptors in the pathophysiology and treatment of mood disorders
  14. Neurotransmitter-based strategies for the treatment of cognitive dysfunction in Down syndrome
  15. Neuroprotective effects of physical activity on the brain: a closer look at trophic factor signaling
  16. Neurobiological Basis of Cognitive Dysfunction in Down Syndrome and Alzheimer's Disease
  17. Formoterol, a Long-Acting β2 Adrenergic Agonist, Improves Cognitive Function and Promotes Dendritic Complexity in a Mouse Model of Down Syndrome
  18. Ascending monoaminergic systems alterations in Alzheimer's disease. Translating basic science into clinical care
  19. Developmental Disabilities - Molecules Involved, Diagnosis, and Clinical Care
  20. Improving noradrenergic signaling in the treatment of cognitive dysfunction in the Ts65Dn mouse model of Down syndrome
  21. BDNF Polymorphism Predicts the Rate of Decline in Skilled Task Performance and Hippocampal Volume in Healthy Individuals (P05.071)
  22. Neurobiological Elements of Cognitive Dysfunction in Down Syndrome: Exploring the Role of APP
  23. Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome
  24. Discoveries in Down syndrome
  25. BDNF polymorphism predicts the rate of decline in skilled task performance and hippocampal volume in healthy individuals
  26. Restoration of Norepinephrine-Modulated Contextual Memory in a Mouse Model of Down Syndrome
  27. Neuroprotection of Host Cells by Human Central Nervous System Stem Cells in a Mouse Model of Infantile Neuronal Ceroid Lipofuscinosis
  28. The "Down Syndrome Critical Region" Is Sufficient in the Mouse Model to Confer Behavioral, Neurophysiological, and Synaptic Phenotypes Characteristic of Down Syndrome
  29. Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of down syndrome
  30. Axonal Transport of Neurotrophic Signals: An Achilles' Heel for Neurodegeneration?
  31. Down Syndrome
  32. P2-308: Examining the effects of (+)-phenserine in Ts65Dn mouse model of down syndrome
  33. Synaptic and cognitive abnormalities in mouse models of down syndrome: Exploring genotype-phenotype relationships
  34. Cholinergic Neurodegeneration in Alzheimer's Disease: Basis for Nerve Growth Factor Therapy
  35. Using mouse models to explore genotype–phenotype relationship in Down syndrome
  36. Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration
  37. P1-032
  38. P1-254 APP and β-amyloid levels in segmental trisomy mouse model of down syndrome
  39. S4-01-03 Trafficking the target-derived signals of neurotrophic factors: implications for normal and degenerating neurons
  40. Alzheimer?s disease and NGF signaling
  41. Synaptic structural abnormalities in the Ts65Dn mouse model of down syndrome
  42. Trafficking the NGF signal: implications for normal and degenerating neurons
  43. Traffic at the intersection of neurotrophic factor signaling and neurodegeneration
  44. Activity of Vasopressinergic Neurones of the Human Supraoptic Nucleus os Age- and Sex-Dependent
  45. Failed retrograde transport of NGF in a mouse model of Down's syndrome: Reversal of cholinergic neurodegenerative phenotypes following NGF infusion
  46. Neurotrophin receptors in Alzheimer brain and A mouse model of down syndrome
  47. Sex- and Age-Related P75 Neurotrophin Receptor Expression in the Human Supraoptic Nucleus
  48. P75 Neurotrophin Receptor in the Nucleus Basalis of Meynert in Relation to Age, Sex, and Alzheimer's Disease
  49. Diminished neuronal metabolic activity in Alzheimer's disease
  50. A sex difference and no effect of ApoE type on the amount of cytoskeletal alterations in the nucleus basalis of Meynert in Alzheimer’s disease
  51. Aggravated decrease in the activity of nucleus basalis neurons in Alzheimer’s disease is apolipoprotein E-type dependent
  52. Limited Effect of Neuritic Plaques on Neuronal Density in the Hippocampal CA1 Area of Alzheimer Patients
  53. Increased expression of the TIAR protein in the hippocampus of Alzheimer patients
  54. Frameshift Mutants of  Amyloid Precursor Protein and Ubiquitin-B in Alzheimer's and Down Patients
  55. Brain Banking in Aging and Dementia Research-the Amsterdam Experience
  56. Chapter 26 Reduced neuronal activity and reactivation in Alzheimer's disease
  57. Chapter 8 Neurotrophin receptors in Alzheimer's disease
  58. Neuropeptides vasopressin (AVP), oxytocin (OXT) and corticotropin-releasing hormone (CRH) in the human hypothalamus: activity changes in aging, Alzheimer’s disease and depressions
  59. Letter to the Editor
  60. Reduced Neuronal Activity is One of the Major Hallmarks of Alzheimer’s Disease
  61. Co-localization of high-affinity neurotrophin receptors in nucleus basalis of Meynert neurons and their differential reduction in Alzheimer's disease
  62. 804 Hallmarks of Alzheimer's disease are independent phenomena
  63. 734 Decreased protein synthetic ability and the neuropathological hallmarks of Alzheimer's disease are independent phenomena
  64. Decreased Activity of Hippocampal Neurons in Alzheimerʼs Disease Is Not Related to the Presence of Neurofibrillary Tangles
  65. Decreased protein synthetic activity of the hypothalamic tuberomamillary nucleus in Alzheimer's disease as suggested by smaller Golgi apparatus
  66. Early cytoskeletal changes as shown by Alz-50 are not accompanied by decreased neuronal activity
  67. Activation of Vasopressin Neurons in Aging and Alzheimer's Disease
  68. Neuronal atrophy, not cell death, is the main hallmark of Alzheimer's disease
  69. Decreased neuronal activity in the nucleus basalis of Meynert in Alzheimer's disease as suggested by the size of the Golgi apparatus