biostudies-literatureBoon BDCNIA NIH HHSAlzheimer NederlandZonMwNational Institute on Aginge13009https://www.ebi.ac.uk/biostudies/studies/S-EPMC12465012biostudies-literatureUnknown50(5)<h4>Aims</h4>Although the neuroanatomical distribution of tau and amyloid-β is well studied in Alzheimer's disease (AD) (non)-amnestic clinical variants, that of neuroinflammation remains unexplored. We investigate the neuroanatomical distribution of activated myeloid cells, astrocytes, and complement alongside amyloid-β and phosphorylated tau in a clinically well-defined prospectively collected AD cohort.<h4>Methods</h4>Clinical variants were diagnosed antemortem, and brain tissue was collected post-mortem. Typical AD (n = 10), behavioural/dysexecutive AD (n = 6), posterior cortical atrophy (PCA) AD (n = 3), and controls (n = 10) were neuropathologically assessed for AD neuropathology, concurrent pathology including Lewy body disease, limbic-predominant age-related TDP-43 encephalopathy nNeuropathology and applied neurobiologyAlzheimer's disease clinical variants show distinct neuroinflammatory profiles with neuropathology.PMC12465012#WE.03-2021-15#WE.06-2023-01#WE.15-2019-13#WE.06‐2023‐017330501041051003212000273305095007R01AG075802R01 AG075802#733050104#WE.15‐2019‐13#WE.03‐2021‐15van der Lee SJGalis-de Graaf YMurray MEBouwman FHBoon BDCvan de Berg WDJHoozemans JJMde Gooijer DJonkman LEMorrema THJHeymans MHolstege HNetherlands Brain BankNormal Aging Brain Collection AmsterdamRozemuller AJMFrigerio IBol JfalseAlzheimer's disease clinical variants show distinct neuroinflammatory profiles with neuropathology.<h4>Aims</h4>Although the neuroanatomical distribution of tau and amyloid-β is well studied in Alzheimer's disease (AD) (non)-amnestic clinical variants, that of neuroinflammation remains unexplored. We investigate the neuroanatomical distribution of activated myeloid cells, astrocytes, and complement alongside amyloid-β and phosphorylated tau in a clinically well-defined prospectively collected AD cohort.<h4>Methods</h4>Clinical variants were diagnosed antemortem, and brain tissue was collected post-mortem. Typical AD (n = 10), behavioural/dysexecutive AD (n = 6), posterior cortical atrophy (PCA) AD (n = 3), and controls (n = 10) were neuropathologically assessed for AD neuropathology, concurrent pathology including Lewy body disease, limbic-predominant age-related TDP-43 encephalopathy n2024-01-01T00:00:00Z2024 Oct2026-06-03T21:22:03.338Z2026-05-01T03:10:58.464ZS-EPMC124650123940035610.1111/nan.13009