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2. Hormone therapy is associated with lower Alzheimer’s disease tau biomarkers in post-menopausal females -evidence from two independent cohorts

3. Tau follows principal axes of functional and structural brain organization in Alzheimer’s disease

4. Comparison of immunoassay- with mass spectrometry-derived p-tau quantification for the detection of Alzheimer’s disease pathology

5. Neuropsychiatric Symptoms and Microglial Activation in Patients with Alzheimer Disease

6. Modeling the progression of neuropsychiatric symptoms in Alzheimer’s disease with PET-based Braak staging

7. Identification of late-stage tau accumulation using plasma phospho-tau217

9. APOEε4 potentiates amyloid β effects on longitudinal tau pathology

10. Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer’s disease

11. Vascular risk burden is a key player in the early progression of Alzheimer’s disease

12. 14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2

13. Astrocyte biomarker signatures of amyloid-β and tau pathologies in Alzheimer’s disease

14. Biomarker modeling of Alzheimer’s disease using PET-based Braak staging

15. Plasma phosphorylated tau181 outperforms [18F] fluorodeoxyglucose positron emission tomography in the identification of early Alzheimer disease.

16. Omics‐derived biological modules reflect metabolic brain changes in Alzheimer's disease.

17. Author Correction: [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease

18. [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease

19. CSF tau368/total-tau ratio reflects cognitive performance and neocortical tau better compared to p-tau181 and p-tau217 in cognitively impaired individuals

20. Microglial activation and tau propagate jointly across Braak stages

21. Predicting functional decline in aging and Alzheimer’s disease with PET-based Braak staging

22. Sex-specific modulation of amyloid-β on tau phosphorylation underlies faster tangle accumulation in females.

23. Sex modulates the role of astrocyte reactivity in preclinical Alzheimer’s disease

24. CSF total tau is more closely associated with synaptic dysfunction than overt neurodegeneration

25. Association of reactive astrogliosis and microglial activation with tau pathology in Alzheimer’s disease

26. Increased regional brain inflammation predicts longitudinal brain atrophy in individuals in the Alzheimer’s disease continuum

27. Plasma p‐tau and brain‐derived total tau biomarkers predict longitudinal changes in Aβ, tau, and cognition across the AD continuum

28. Neuroinflammation Exacerbates Irritability and Agitation in Alzheimer’s Disease

29. Mapping the effects of functional and structural network reorganization on the tau‐cognition relationship in Alzheimer’s disease

30. Amyloid β‐dependent tau phosphorylation is triggered by reactive astrocytes in preclinical Alzheimer’s disease

31. Plasma biomarkers as stand‐alone tests in the diagnosis of Alzheimer’s disease

32. APOEε4 potentiates the effects of Aβ pathology on the deposition of neurofibrillary tangles via tau phosphorylation

33. Interactions of synaptic and inflammatory biomarkers in Alzheimer’s Disease

34. Assessment of brain oxygen extraction in aging and Alzheimer’s disease with MRI images

35. Amyloid and Tau Predominance Subtyping Identifies CI Patients With Different Clinical Phenotypes

36. Fast accumulators of tau have higher levels of plasma pTau and stronger associations with amyloid in later Braak regions at baseline

37. The impact of young controls in the detection of tau load in cognitively impaired and asymptomatic elderly

38. Microglial activation interacts with amyloid‐β to drive longitudinal tau tangle accumulation and cognitive decline

39. Astrocyte reactivity is associated with synaptic dysfunction across the aging and Alzheimer’s disease spectrum, whereas microglial reactivity is specifically associated with synaptic dysfunction related to cognitive impairment

40. Potential utility of using both APOEε4 and Aβ positivity to enrich clinical trials of tau‐targeting therapies

41. Sex impacts the association of plasma Glial Fibrillary Acidic Protein with neurodegeneration in Alzheimer’s disease

42. Plasma biomarkers of tau for the differentiation between slow and fast tau‐PET accumulators

43. Increased Genetic Risk for ADHD Potentiates Cognitive Impairment and Brain Hypometabolism in Alzheimer’s Disease Patients

44. Microglial Activation Contributes to Neuropsychiatric Dysfunction in Alzheimer’s Disease

45. Astrocyte reactivity potentiates longitudinal tau tangle accumulation in cognitively unimpaired individuals

46. Synapse dysfunction and astrocyte reactivity are associated independently of amyloid‐β and tau pathologies

47. Plasma p‐tau181 and nfl as surrogates biomarkers in clinical trials targeting preclinical stage of Alzheimer’s disease

48. Employing transfer learning to optimize deep learning models for Alzheimer’s disease classification using two tau PET tracers

49. Independent associations of plasma GFAP with amyloid‐β and tau in Alzheimer’s disease

50. Plasma p‐tau231 and p‐tau217 provides information on tau tangle deposition in symptomatic Alzheimer’s disease individuals

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