Ical trials. Extra filesAdditional file 1: Table S1. Visual assessment (present/absent) of selected co-pathologies. (DOCX 16 kb) Extra file two: Table S2. Biochemical measures of A1-40, A1-42, Ptau and T-tau (pg/mL) in MTG brain homogenate fractions (TBS [T], SDS [S] and Formic acid [F]) for each CTL and AD subjects. The total fraction will be the sum of all homogenate fractions. (DOCX 15 kb) Acknowledgments This study represents independent study partly funded by the National Institute for Well being Analysis (NIHR) BioFGF-9 Protein Human Medical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London. Tissue samples have been supplied by The London Neurodegenerative Illnesses Brain Bank, which receives funding in the UK Medical Study VEGFR-2 Protein HEK 293 Council and as a part of the Brains for Dementia Investigation programme, jointly funded by Alzheimer’s Analysis UK and also the Alzheimer’s Society. The views expressed are those of the authors and not necessarily those from the NHS, the NIHR or the Division of Health. The datasets utilized and/or analysed throughout the current study out there from the corresponding author on reasonable request. NJA is funded by the Wallenburg Centre for Molecular and Translational Medicine. TH is supported by a grant from the Hungarian Brain Research Plan. MS has received funding from the Knut och Alice Wallenberg Foundation (the Wallenberg Centre for Molecular and Translational Medicine), the Swedish Analysis Council as well as the Swedish Alzheimer Foundation. KB holds the Torsten S erberg Professorship in Medicine and is supported by grants from the Swedish Research Council, the Swedish Alzheimer Foundation, as well as the Swedish Brain Foundation. HZ is really a Wallenberg Academy Fellow supported by grants from the Swedish Study Council, the European Analysis Council and the UK Dementia Research Institute at UCL. AH is funded by Investigation Centre for Mental Overall health and Biomedical Study Unit for Dementia. Authors’ contributions NJA, AL and AH designed the notion and style. All authors contributed to sample choice and/or interpretation of data. Information acquisition was performed by NJA, YML and AH. NJA and AL, carried out data analysis and interpretation. NJA, AL, KB, HZ, AH drafted the manuscript and all authors revised. All authors read and approved the final manuscript. Competing interests KB and HZ are co-founders of Brain Biomarker Solutions in Gothenburg AB, a GU Ventures-based platform organization at the University of Gothenburg. KB has served as a consultant or at advisory boards for Alzheon, Eli Lilly, Fujirebio Europe, IBL International, Novartis and Roche Diagnostics. HZ has served at advisory boards of Eli Lilly and Roche Diagnostics and has received travel help from TEVA. SL is an employee of Johnson and Johnson.Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Author information 1 Division of Psychiatry and Neurochemistry, Institute of Neuroscience Physiology, the Sahlgrenska Academy in the University of Gothenburg,Ashton et al. Acta Neuropathologica Communications(2019) 7:Web page 10 ofM ndal, Sweden. 2Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden. 3King’s College London, Institute of Psychiatry, Psychology Neuroscience, Maurice Wohl Clinical Neuroscience Institute, London, UK. 4NIHR Biomedical Study Centre for Mental Wellness Biomedical Analysis Unit for Dementia at South Lond.