The Relationship between p-tau217, p-tau231, and p-tau205 in the Human Brain Is Affected by the Cellular Environment and Alzheimer’s Disease Pathology.

11 June, 2024

Cells. 2024 Feb 11;13(4):331. doi: 10.3390/cells13040331.PMID: 38391945 Free PMC article.

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Highly Accurate Blood Test for Alzheimer’s Disease Comparable or Superior to Clinical CSF Tests.

Nat Med. 2024 Feb 21. doi: 10.1038/s41591-024-02869-z. Online ahead of print.PMID: 38382645

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Diffusion weighted magnetic resonance spectroscopy revealed neuronal specific microstructural alterations in Alzheimer’s disease.

Brain Commun. 2024 Feb 1;6(1):fcae026. doi: 10.1093/braincomms/fcae026. eCollection 2024.PMID: 38370447 Free PMC article.

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Putaminal T1/T2-weighted ratio is increased in PSP compared to PD and healthy controls, a multi-cohort study.

Parkinsonism Relat Disord. 2024 Feb 13;121:106047. doi: 10.1016/j.parkreldis.2024.106047. Online ahead of print.PMID: 38368753 Free article.

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Plasma N-terminal containing tau fragments (NTA-tau): a biomarker of tau deposition in Alzheimer’s Disease.

Mol Neurodegener. 2024 Feb 17;19(1):19. doi: 10.1186/s13024-024-00707-x.PMID: 38365825 Free PMC article.

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Effects of certain pre-analytical factors on the performance of plasma phospho-tau217.

Alzheimers Res Ther. 2024 Feb 8;16(1):31. doi: 10.1186/s13195-024-01391-1.PMID: 38331843 Free PMC article.

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Cerebrospinal fluid biomarker panel for synaptic dysfunction in a broad spectrum of neurodegenerative diseases.

Brain. 2024 Feb 7:awae032. doi: 10.1093/brain/awae032. Online ahead of print.PMID: 38325331

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Demographic, clinical, biomarker, and neuropathological correlates of posterior cortical atrophy: an international cohort study and individual participant data meta-analysis.

Lancet Neurol. 2024 Feb;23(2):168-177. doi: 10.1016/S1474-4422(23)00414-3.PMID: 38267189 Free article.

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

Mol Neurodegener. 2024 Jan 7;19(1):2. doi: 10.1186/s13024-023-00689-2.PMID: 38185677 Free PMC article.

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The fluorescent ligand bTVBT2 reveals increased p-tau uptake by retinal microglia in Alzheimer’s disease patients and AppNL-F/NL-F mice.

M.Alzheimers Res Ther. 2024 Jan 2;16(1):4. doi: 10.1186/s13195-023-01375-7.PMID: 38167557 Free PMC article.

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Diffusion MRI tracks cortical microstructural changes during the early stages of Alzheimer’s disease.

Brain. 2024 Mar 1;147(3):961-969. doi: 10.1093/brain/awad428.PMID: 38128551 Free PMC article.

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Harnessing cognitive trajectory clusterings to examine subclinical decline risk factors.

Brain Commun. 2023 Dec 3;5(6):fcad333. doi: 10.1093/braincomms/fcad333. eCollection 2023.PMID: 38107504 Free PMC article.

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Plasma Biomarker Strategy for Selecting Patients With Alzheimer Disease for Antiamyloid Immunotherapies.

JAMA Neurol. 2024 Jan 1;81(1):69-78. doi: 10.1001/jamaneurol.2023.4596.PMID: 38048096

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The molecular genetic landscape of human brain size variation.

Cell Rep. 2023 Nov 28;42(11):113439. doi: 10.1016/j.celrep.2023.113439. Epub 2023 Nov 14.PMID: 37963017 Free article.

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The α-synuclein PET tracer [18F] ACI-12589 distinguishes multiple system atrophy from other neurodegenerative diseases.

Nat Commun. 2023 Oct 27;14(1):6750. doi: 10.1038/s41467-023-42305-3.PMID: 37891183 Free PMC article.

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Combined Connectomics, MAPT Gene Expression, and Amyloid Deposition to Explain Regional Tau Deposition in Alzheimer Disease.

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Effects of Brain Pathologies on Spatiotemporal Gait Parameters in Patients with Mild Cognitive Impairment.

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DOPA decarboxylase is an emerging biomarker for Parkinsonian disorders including preclinical Lewy body disease.

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Interactions between vascular burden and amyloid-β pathology on trajectories of tau accumulation.

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Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer’s disease pathology.

11 September, 2023

Nat Aging. 2022 Dec;2(12):1138-1144. doi: 10.1038/s43587-022-00310-z.

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Associations of CSF PDGFRβ With Aging, Blood-Brain Barrier Damage, Neuroinflammation, and Alzheimer Disease Pathologic Changes.

Neurology. 2023 Jul 4;101(1):e30-e39. doi: 10.1212/WNL.0000000000207358.

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Comparison of Group-Level and Individualized Brain Regions for Measuring Change in Longitudinal Tau Positron Emission Tomography in Alzheimer Disease.

Alzheimer’s Disease Neuroimaging Initiative. JAMA Neurol. 2023 Jun 1;80(6):614-623. doi: 10.1001/jamaneurol.2023.1067.

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Higher plasma β-synuclein indicates early synaptic degeneration in Alzheimer’s disease.

Alzheimers Dement. 2023 Apr 27. doi: 10.1002/alz.13103

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Clinical Utility of Tau Positron Emission Tomography in the Diagnostic Workup of Patients With Cognitive Symptoms.

JAMA Neurol. 2023 Jul 1;80(7):749-756. doi: 10.1001/jamaneurol.2023.1323.

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Plasma neurofilament light in behavioural variant frontotemporal dementia compared to mood and psychotic disorders.

Aust N Z J Psychiatry. 2023 Jul 21:48674231187312. doi: 10.1177/00048674231187312.

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Genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets.

Nat Immunol. 2023 Sep;24(9):1540-1551. doi: 10.1038/s41590-023-01588-w.

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Blood biomarkers for Alzheimer’s disease in clinical practice and trials.

11 August, 2023

Nat Aging. 2023 May;3(5):506-519. doi: 10.1038/s43587-023-00403-3

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CSF tau phosphorylation occupancies at T217 and T205 represent improved biomarkers of amyloid and tau pathology in Alzheimer’s disease.

12 June, 2023

Nat Aging. 2023 Apr;3(4):391-401. doi: 10.1038/s43587-023-00380-7.

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Age-related and amyloid-beta-independent tau deposition and its downstream effects.

Brain. 2023 Aug 1;146(8):3192-3205. doi: 10.1093/brain/awad135.

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Cerebral Aβ deposition precedes reduced cerebrospinal fluid and serum Aβ42/Aβ40 ratios in the AppNL-F/NL-F knock-in mouse model of Alzheimer’s disease.

Alzheimers Res Ther. 2023 Mar 25;15(1):64. doi: 10.1186/s13195-023-01196-8.

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Plasma amyloid-β42/40 and apolipoprotein E for amyloid PET pre-screening in secondary prevention trials of Alzheimer’s disease.

Brain Commun. 2023 Jan 24;5(2):fcad015. doi: 10.1093/braincomms/fcad015. eCollection 2023.

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Associations Between CSF Markers of Inflammation, White Matter Lesions, and Cognitive Decline in Individuals Without Dementia.

Neurology. 2023 Apr 25;100(17):e1812-e1824. doi: 10.1212/WNL.0000000000207113.

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Prediction of Longitudinal Cognitive Decline in Preclinical Alzheimer Disease Using Plasma Biomarkers.

JAMA Neurol. 2023 Apr 1;80(4):360-369. doi: 10.1001/jamaneurol.2022.5272.

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Discriminative accuracy of the A/T/N scheme to identify cognitive impairment due to Alzheimer’s disease.

Alzheimers Dement (Amst). 2023 Jan 30;15(1):e12390. doi: 10.1002/dad2.12390.

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Robustness of CSF Aβ42/40 and Aβ42/P-tau181 measured using fully automated immunoassays to detect AD-related outcomes.

O. Alzheimers Dement. 2023 Jul;19(7):2994-3004. doi: 10.1002/alz.12897.

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Optimal combinations of CSF biomarkers for predicting cognitive decline and clinical conversion in cognitively unimpaired participants and mild cognitive impairment patients: A multi-cohort study.

Alzheimers Dement. 2023 Jul;19(7):2943-2955. doi: 10.1002/alz.12907.

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Tau-PET is superior to phospho-tau when predicting cognitive decline in symptomatic AD patients.

Alzheimers Dement. 2023 Jun;19(6):2497-2507. doi: 10.1002/alz.12875.

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Novel insights regarding the measurement properties of the SCOPA-AUT.

BMC Neurol. 2022 Dec 13;22(1):478. doi: 10.1186/s12883-022-03008-2.

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[18F]RO948 tau positron emission tomography in genetic and sporadic frontotemporal dementia syndromes.

Eur J Nucl Med Mol Imaging. 2023 Apr;50(5):1371-1383. doi: 10.1007/s00259-022-06065-4.

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Antibody-free measurement of cerebrospinal fluid tau phosphorylation across the Alzheimer’s disease continuum.

Mol Neurodegener. 2022 Dec 12;17(1):81. doi: 10.1186/s13024-022-00586-0.

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The genetic regulation of protein expression in cerebrospinal fluid.

EMBO Mol Med. 2023 Jan 11;15(1):e16359. doi: 10.15252/emmm.202216359.

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Cerebrospinal Fluid Biomarkers of Synaptic Dysfunction are Altered in Parkinson’s Disease and Related Disorders.

Mov Disord. 2023 Feb;38(2):267-277. doi: 10.1002/mds.29287.

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Performance of [18F]RO948 PET, MRI and CSF neurofilament light in the differential diagnosis of progressive supranuclear palsy.

Parkinsonism Relat Disord. 2023 Jan;106:105226. doi: 10.1016/j.parkreldis.2022.11.018.

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Gray matter hypoperfusion is a late pathological event in the course of Alzheimer’s disease.

J Cereb Blood Flow Metab. 2023 Apr;43(4):565-580. doi: 10.1177/0271678X221141139.

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CSF ferritin in the clinicopathological progression of Alzheimer’s disease and associations with APOE and inflammation biomarkers.

J Neurol Neurosurg Psychiatry. 2023 Mar;94(3):211-219. doi: 10.1136/jnnp-2022-330052.

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Amyloid-associated increases in soluble tau relate to tau aggregation rates and cognitive decline in early Alzheimer’s disease.

Nat Commun. 2022 Nov 4;13(1):6635. doi: 10.1038/s41467-022-34129-4.

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Second-generation Elecsys cerebrospinal fluid immunoassays aid diagnosis of early Alzheimer’s disease.

Clin Chem Lab Med. 2022 Oct 24;61(2):234-244. doi: 10.1515/cclm-2022-0516.

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Axonal degeneration and amyloid pathology predict cognitive decline beyond cortical atrophy.

Alzheimers Res Ther. 2022 Oct 4;14(1):144. doi: 10.1186/s13195-022-01081-w.

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Higher levels of myelin are associated with higher resistance against tau pathology in Alzheimer’s disease.

Alzheimers Res Ther. 2022 Sep 24;14(1):139. doi: 10.1186/s13195-022-01074-9.

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Confounding factors of Alzheimer’s disease plasma biomarkers and their impact on clinical performance.

Alzheimers Dement. 2023 Apr;19(4):1403-1414. doi: 10.1002/alz.12787.

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Clinical performance and robustness evaluation of plasma amyloid-β42/40prescreening.

Alzheimers Dement. 2023 Apr;19(4):1393-1402. doi: 10.1002/alz.12801.

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Measures of cortical microstructure are linked to amyloid pathology in Alzheimer’s disease.

Brain. 2023 Apr 19;146(4):1602-1614. doi: 10.1093/brain/awac343.

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Head-to-head comparison of 10 plasma phospho-tau assays in prodromal Alzheimer’s disease.

Brain. 2023 Apr 19;146(4):1592-1601. doi: 10.1093/brain/awac333.

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Phospho-tau with subthreshold tau-PET predicts increased tau accumulation rates in amyloid-positive individuals.

Brain. 2023 Apr 19;146(4):1580-1591. doi: 10.1093/brain/awac329.

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Anterior cingulate sulcation is associated with onset and survival in frontotemporal dementia.

medRxiv. 2023 Mar 31:2023.03.30.23287945. doi: 10.1101/2023.03.30.23287945.

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Mitigating the Associations of Kidney Dysfunction With Blood Biomarkers of Alzheimer Disease by Using Phosphorylated Tau to Total Tau Ratios.

JAMA Neurol. 2023 May 1;80(5):516-522. doi: 10.1001/jamaneurol.2023.0199.

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Structural and functional neuroimaging changes associated with cognitive impairment and dementia in Parkinson’s disease.

30 June, 2021

Abstract This study seeks a better understanding of possible pathophysiological mechanisms associated with cognitive impairment and dementia in Parkinson’s disease using structural and functional MRI. We investigated resting-state functional connectivity of important subdivisions of the caudate nucleus, putamen and thalamus, and also how the morphology of these structures are impacted in the disorder. We found

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Prediction of future Alzheimer’s disease dementia using plasma phospho-tau combined with other accessible measures

24 June, 2021

Abstract A combination of plasma phospho-tau (P-tau) and other accessible biomarkers might provide accurate prediction about the risk of developing Alzheimer’s disease (AD) dementia. We examined this in participants with subjective cognitive decline and mild cognitive impairment from the BioFINDER (n = 340) and Alzheimer’s Disease Neuroimaging Initiative (ADNI) (n = 543) studies. Plasma P-tau,

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Early stages of tau pathology and its associations with functional connectivity, atrophy and memory.

30 April, 2021

Abstract In Alzheimer’s disease, postmortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with area 35, and the entorhinal cortex. Here we used tau-PET imaging to investigate the sequence of tau pathology progression within the human medial

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Association of Enlarged Perivascular Spaces and Measures of Small Vessel and Alzheimer Disease.

3 February, 2021

Abstract Objective: To investigate the relationship between enlarged perivascular spaces (EPVS) and measures of Alzheimer disease (AD), small vessel disease (SVD), cognition, vascular risk factors, and neuroinflammation, we tested associations between EPVS and different relevant neuroimaging, biochemical, and cognitive variables in 778 study participants. Methods: Four hundred ninety-nine cognitively unimpaired (CU) individuals, 240 patients with mild cognitive

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Pre-analytical protocol for measuring Alzheimer’s disease biomarkers in fresh CSF.

Abstract Introduction: We aimed to establish a standardized, routine-use pre-analytical protocol for measuring Alzheimer’s disease (AD) biomarkers in cerebrospinal fluid (CSF). Methods: The effect of pre-analytical factors (sample collection/handling/storage/transportation) on biomarker levels was assessed using freshly collected CSF. Tube type/sterilization was assessed using previously frozen samples. A low-bind false-bottom tube (FBT, Sarstedt) was used for all experiments,

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Increasing the reproducibility of fluid biomarker studies in neurodegenerative studies.

Abstract Biomarkers have revolutionized scientific research on neurodegenerative diseases, in particular Alzheimer’s disease, transformed drug trial design, and are also increasingly improving patient management in clinical practice. A few key cerebrospinal fluid biomarkers have been robustly associated with neurodegenerative diseases. Several novel biomarkers are very promising, especially blood-based markers. However, many biomarker findings have had

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Longitudinal plasma p-tau217 is increased in early stages of Alzheimer’s disease.

29 January, 2021

Abstract Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer’s disease. We studied 150 cognitively unimpaired participants and 100 patients with mild cognitive impairment in the Swedish BioFINDER study. P-tau217 was measured repeatedly for up to 6 years (median three samples per person, median time from first to last

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Untangling the association of amyloid-β and tau with synaptic and axonal loss in Alzheimer’s disease.

Abstract It is currently unclear how amyloid-β and tau deposition are linked to changes in synaptic function and axonal structure over the course of Alzheimer’s disease. Here, we assessed these relationships by measuring presynaptic (synaptosomal-associated protein 25, SNAP25; growth-associated protein 43, GAP43), postsynaptic (neurogranin, NRGN) and axonal (neurofilament light chain) markers in the CSF of

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The accumulation rate of tau aggregates is higher in females and younger amyloid-positive subjects.

Abstract The development of tau-PET allows paired helical filament tau pathology to be visualized in vivo. Increased knowledge about conditions affecting the rate of tau accumulation could guide the development of therapies halting the progression of Alzheimer’s disease. However, the factors modifying the rate of tau accumulation over time in Alzheimer’s disease are still largely

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Derivation and utility of an Aβ-PET pathology accumulation index to estimate Aβ load.

Abstract Objective: To evaluate a novel β-amyloid (Aβ)-PET-based quantitative measure (Aβ accumulation index ), including the assessment of its ability to discriminate between participants based on Aβ status using visual read, CSF Aβ42/Aβ40, and post-mortem neuritic plaque burden as standards of truth. Methods: One thousand one hundred twenty-one participants (with and without cognitive impairment) were scanned

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Associations of Plasma Phospho-Tau217 Levels With Tau Positron Emission Tomography in Early Alzheimer Disease

Abstract Importance: There is an urgent need for inexpensive and minimally invasive blood biomarkers for Alzheimer disease (AD) that could be used to detect early disease changes. Objective: To assess how early in the course of AD plasma levels of tau phosphorylated at threonine 217 (P-tau217) start to change compared with levels of established cerebrospinal fluid (CSF)

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Discriminative Accuracy of Plasma Phospho-tau217 for Alzheimer Disease vs Other Neurodegenerative Disorders

28 July, 2020

Importance: There are limitations in current diagnostic testing approaches for Alzheimer disease (AD). Objective: To examine plasma tau phosphorylated at threonine 217 (P-tau217) as a diagnostic biomarker for AD. Design, Setting, and Participants: Three cross-sectional cohorts: an Arizona-based neuropathology cohort (cohort 1), including 34 participants with AD and 47 without AD (dates of enrollment, May 2007-January 2019); the

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Plasma P-tau181 in Alzheimer’s disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer’s dementia

24 July, 2020

Plasma phosphorylated tau181 (P-tau181) might be increased in Alzheimer’s disease (AD), but its usefulness for differential diagnosis and prognosis is unclear. We studied plasma P-tau181 in three cohorts, with a total of 589 individuals, including cognitively unimpaired participants and patients with mild cognitive impairment (MCI), AD dementia and non-AD neurodegenerative diseases. Plasma P-tau181 was increased

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Assessment of Demographic, Genetic, and Imaging Variables Associated With Brain Resilience and Cognitive Resilience to Pathological Tau in Patients With Alzheimer Disease

Importance Better understanding is needed of the degree to which individuals tolerate Alzheimer disease (AD)–like pathological tau with respect to brain structure (brain resilience) and cognition (cognitive resilience). Objective To examine the demographic (age, sex, and educational level), genetic (APOE-ε4 status), and neuroimaging (white matter hyperintensities and cortical thickness) factors associated with interindividual differences in

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Midlife Atherosclerosis and Development of Alzheimer or Vascular Dementia

Objective To investigate whether midlife atherosclerosis is associated with different dementia subtypes and related underlying pathologies. Methods Participants comprised the cardiovascular cohort of the Swedish prospective population‐based Malmö Diet and Cancer Study (N = 6,103). Carotid plaques and intima media thickness (IMT) were measured at baseline (1991–1994). Dementia incidence until 2014 was obtained from national

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Distinct tau PET patterns in atrophy-defined subtypes of Alzheimer’s disease

Introduction: Differential patterns of brain atrophy on structural magnetic resonance imaging (MRI) revealed four reproducible subtypes of Alzheimer’s disease (AD): (1) “typical”, (2) “limbic-predominant”, (3) “hippocampal-sparing”, and (4) “mild atrophy”. We examined the neurobiological characteristics and clinical progression of these atrophy-defined subtypes. Methods: The four subtypes were replicated using a clustering method on MRI data

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Discriminative Accuracy of [18F]flortaucipir Positron Emission Tomography for Alzheimer Disease vs Other Neurodegenerative Disorders.

8 November, 2018

Importance: The positron emission tomography (PET) tracer flortaucipir allows in vivo quantification of paired helical filament tau, a core neuropathological feature of Alzheimer disease (AD), but its diagnostic utility is unclear. Objective: To examine the discriminative accuracy of flortaucipir for AD vs non-AD neurodegenerative disorders. Design, Setting, and Participants: In this cross-sectional study, 719 participants

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Molecular properties underlying regional vulnerability to Alzheimer’s disease pathology.

Amyloid deposition and neurofibrillary degeneration in Alzheimer’s disease specifically affect discrete neuronal systems, but the underlying mechanisms that render some brain regions more vulnerable to Alzheimer’s disease pathology than others remain largely unknown. Here we studied molecular properties underlying these distinct regional vulnerabilities by analysing Alzheimer’s disease-typical neuroimaging patterns of amyloid deposition and neurodegeneration in

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CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease.

OBJECTIVE: To measure CSF levels of biomarkers reflecting microglia and astrocytes activation, neuroinflammation, and cerebrovascular changes and study their associations with the core biomarkers of Alzheimer disease (AD) pathology (β-amyloid and tau), structural imaging correlates, and clinical disease progression over time. METHODS: The study included cognitively unimpaired elderly (n = 508), patients with mild

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Comparing 18F-AV-1451 with CSF T-tau and P-tau for diagnosis of Alzheimer’s disease. 

16 April, 2018

OBJECTIVE: To compare PET imaging of tau pathology with CSF measurements (total tau and phosphorylated tau ) in terms of diagnostic performance for Alzheimer disease (AD). METHODS: We compared t-tau and p-tau and 18F-AV-1451 in 30 controls, 14 patients with prodromal AD, and 39 patients with Alzheimerdementia, recruited from the Swedish BioFINDER study. All

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CSF biomarkers of Alzheimer’s disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in BioFINDER and ADNI cohorts.

INTRODUCTION: We studied whether fully automated Elecsys cerebrospinal fluid (CSF) immunoassay results were concordant with positron emission tomography (PET) and predicted clinical progression, even with cutoffs established in an independent cohort. METHODS: Cutoffs for Elecsys amyloid-β1-42 (Aβ), total tau/Aβ(1-42), and phosphorylated tau/Aβ(1-42) were defined against flutemetamol PET in Swedish BioFINDER (n = 277) and validated against florbetapir

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Increased midlife triglycerides predict brain β-amyloid and tau pathology 20 years later

OBJECTIVE: To evaluate the effect of midlife lipid levels on Alzheimer brain pathology 20 years later in cognitively normal elderly individuals. METHODS: This is a longitudinal cohort study of 318 cognitively normal individuals with data on fasting lipid levels at midlife (mean age 54 years). Presence of β-amyloid (Aβ) and tau pathologies 20 years later

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Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity.

25 August, 2017

Abstract It is not known exactly where amyloid-β (Aβ) fibrils begin to accumulate in individuals with Alzheimer’s disease (AD). Recently, we showed that abnormal levels of Aβ42 in cerebrospinal fluid (CSF) can be detected before abnormal amyloid can be detected using PET in individuals with preclinical AD. Using these approaches, here we identify the earliest

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Performance of Different Amyloid Immunoassays in Predicting Outcome of Visual Assessment of Amyloid PET Imaging

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Cerebral hypoperfusion is not associated with an increase in amyloid β pathology in middle-aged or elderly people.

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Distinct 18F-AV-1451 tau PET retention patterns in early- and late-onset Alzheimer’s disease

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18F-AV-1451 and CSF T-tau and P-tau as biomarkers in Alzheimer’s disease.

9 August, 2017

18F-AV-1451 and CSF T-tau and P-tau as biomarkers in Alzheimer’s disease.

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The interactive effect of demographic and clinical factors on hippocampal volume: A multicohort study on 1958 cognitively normal individuals.

27 June, 2017

The interactive effect of demographic and clinical factors on hippocampal volume: A multicohort study on 1958 cognitively normal individuals.

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Blood-based NfL: A biomarker for differential diagnosis of parkinsonian disorder

13 March, 2017

Neurology. 2017 Mar 7;88(10):930-937

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Systematic development of small molecules to inhibit specific microscopic steps of Aβ42 aggregationn in Alzheimer´s disease

Proc Natl Acad Sci U S A. 2017 Jan 10;114(2):E200-E208. doi: 10.1073/pnas.1615613114.

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Tau neuropathology correlates with FDG-PET, but not AV-1451-PET, in progressive supranuclear palsy

21 December, 2016

Acta Neuropathol. 2016 Nov 29. No abstract available.

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Modeling strategies for quantification of in vivo 18F-AV1451 binding in patients with tau pathology

27 October, 2016

J Nuci Med.  2016 Oct 20. pii: jnumed.116.174508. Abstract Aggregation of hyperphosphorylated tau is a major hallmark of many neurodegenerative diseases, including Alzheimer’s disease. In vivo imaging with positron emission tomography (PET) may offer important insights in pathophysiological mechanisms, diagnosis and disease progression. We describe different strategies for quantification of 18F-AV1451

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Plasma tau in Alzheimer disease

See comment in PubMed Commons below, Neurology 2016 Oct 25;87(17):1827-1835. Epub 2016 Sep 30.   Abstract OBJECTIVE: To test whether plasma tau is altered in Alzheimer disease (AD) and whether it is related to changes in cognition, CSF biomarkers of AD pathology (including β-amyloid and tau), brain atrophy, and brain metabolism. METHODS: This was

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Increased basal ganglia binding of 18 F-AV-1451 in patients with progressive supranuclear palsy

17 October, 2016

Abstract BACKGROUND: Progressive supranuclear palsy (PSP) is difficult to diagnose accurately. The recently developed tau PET tracers may improve the diagnostic work-up of PSP. METHODS: Regional tau accumulation was studied using 18 F-AV-1451 PET in 11 patients with PSP and 11 age-matched healthy controls in the Swedish BioFinder study. RESULTS: 18 F-AV-1451 standard uptake volume

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Reply: Do we still need positron emission tomography for early Alzheimer’s disease diagnosis?

10 October, 2016

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18F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers.

Abstract Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with (18)F-AV-1451 in three patients harbouring a p.R406W mutation in

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Alterations of Diffusion Kurtosis and Neurite Density Measures in Deep Grey Matter and White Matter in Parkinson’s Disease.

In Parkinson’s disease (PD), pathological microstructural changes occur and such changes might be detected using diffusion magnetic resonance imaging (dMRI). However, it is unclear whether dMRI improves PD diagnosis or helps differentiating between phenotypes, such as postural instability gait difficulty (PIGD) and tremor dominant (TD) PD. We included 105 patients with PD and 44 healthy

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Brain activity and Alzheimer’s disease: a complex relationship.

Author information 11 Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Sweden 2 Memory Clinic, Skåne University Hospital, Sweden Oskar.Hansson@med.lu.se. 23 Experimental Dementia Unit, Department of Experimental Medicine Sciences, Lund University, Sweden.

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Reference measurement procedure for CSF amyloid beta (Aβ)1-42 and the CSF Aβ1-42 /Aβ1-40 ratio – a cross-validation study against amyloid PET.

Abstract A clinical diagnosis of Alzheimer’s disease is currently made on the basis of results from cognitive tests in combination with medical history and general clinical evaluation, but the peptide amyloid-beta (Aβ) in cerebrospinal fluid (CSF) is increasingly used as a biomarker for amyloid pathology in clinical trials and in recently proposed revised clinical criteria

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Optimized Standard Operating Procedures for the Analysis of Cerebrospinal Fluid Aβ42 and the Ratios of Aβ Isoforms Using Low Protein Binding Tubes.

Abstract BACKGROUND: Reduced cerebrospinal fluid (CSF) concentration of amyloid-β1-42 (Aβ1-42) reflects the presence of amyloidopathy in brains of subjects with Alzheimer’s disease (AD). OBJECTIVE: To qualify the use of Aβ1-42/Aβ1-40 for improvement of standard operating procedures (SOP) for measurement of CSF Aβ with a focus on CSF collection, storage, and analysis. METHODS: Euroimmun ELISAs for

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A Genetic Variant of the Sortilin 1 Gene is Associated with Reduced Risk of Alzheimer’s Disease.

Abstract Alzheimer’s disease (AD) is a neurodegenerative disorder represented by the accumulation of intracellular tau protein and extracellular deposits of amyloid-β (Aβ) in the brain. The gene sortilin 1 (SORT1) has previously been associated with cardiovascular disease in gene association studies. It has also been proposed to be involved in AD pathogenesis through facilitating Aβ

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CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios improve the diagnostic accuracy for Alzheimer’s disease. 

13 June, 2016

Ann Clin Transl Neurol. 2016 Jan 1;3(3):154-65.

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Plasma β-amyloid in Alzheimer’s disease and vascular disease

10 May, 2016

Implementation of amyloid biomarkers in clinical practice would be accelerated if such biomarkers could be measured in blood. We analyzed plasma levels of Aβ42 and Aβ40 in a cohort of 719 individuals (the Swedish BioFINDER study), including patients with subjective cognitive decline (SCD), mild cognitive impairment (MCI), Alzheimer’s disease (AD) dementia and cognitively healthy elderly,

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Cerebrospinal fluid levels of IL-6 are decreased and correlate with cognitive status in DLB patients.

29 April, 2016

INTRODUCTION: Inflammatory processes have previously been shown to influence cognition and progression of dementia. An involvement of interleukin (IL)-6 has in particular been suggested as altered levels of IL-6 in cerebrospinal fluid (CSF) have been found in patients with Alzheimer’s disease (AD). Also, an association between cognitive decline and levels of IL-6 in CSF have

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Extrapolation-Based References Improve Motion and Eddy-Current Correction of High B-Value DWI Data: Application in Parkinson’s Disease Dementia.

PURPOSE: Conventional motion and eddy-current correction, where each diffusion-weighted volume is registered to a non diffusion-weighted reference, suffers from poor accuracy for high b-value data. An alternative approach is to extrapolate reference volumes from low b-value data. We aim to compare the performance of conventional and extrapolation-based correction of diffusional kurtosis imaging (DKI) data, and

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Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer’s Disease Patient with Presenilin-1 Mutation.

Abstract It is unclear whether the distribution of tau pathology differs between cases with early-onset familial Alzheimer’s disease (AD) and sporadic AD. We present positron emission tomography (PET) data from a young patient with a presenilin-1 mutation (Thr116Asn). 18F-flutemetamol PET showed a distribution of amyloid-β fibrils similar to sporadic AD. However, the pattern of tau

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Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography.

ABSTRACT Cerebral accumulation of amyloid-β is thought to be the starting mechanism in Alzheimer’s disease. Amyloid-β can be detected by analysis of cerebrospinal fluid amyloid-β42or amyloid positron emission tomography, but it is unknown if any of the methods can identify an abnormal amyloid accumulation prior to the other. Our aim was to determine whether cerebrospinal

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Cerebrospinal fluid soluble TREM2 in aging and Alzheimer’s disease.

BACKGROUND: Alzheimer’s disease (AD) neuropathology is associated with neuroinflammation, but there are few useful biomarkers. Mutant variants of triggering receptor expressed on myeloid cells 2 (TREM2) have recently been linked to late-onset AD and other neurodegenerative disorders. TREM2, a microglial receptor, is involved in innate immunity. A cleaved fragment, soluble TREM2 (sTREM2), is present in

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Longitudinal cerebrospinal fluid biomarker measurements in preclinical sporadic Alzheimer’s disease: A prospective 9-year study

Introduction Ascertainment of the pattern and temporal change of biomarkers in preclinical (asymptomatic) sporadic Alzheimer’s disease (AD) will increase knowledge about early pathogenesis and facilitate interventional therapeutic trials. Methods In this prospective longitudinal study, repeated cerebrospinal fluid (CSF) collections and cognitive evaluations were performed in cognitively healthy elderly individuals during a 9-year period. Results Low

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Longitudinal Measurements of Cerebrospinal Fluid Biomarkers in Parkinson’s Disease.

OBJECTIVE: The purpose of this study was to investigate whether cerebrospinal fluid (CSF) levels of tau, phosphorylated tau, β-amyloid42 , α-synuclein, neurofilament light, and YKL-40 change over time and if changes correlate with motor progression and/or cognitive decline in patients with PD and controls. METHODS: We included 63 patients with PD (nondemented) and 21 neurologically

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Increased amyloidogenic APP processing in APOE ɛ4-negative individuals with cerebral β-amyloidosis

Abstract Increased APP (amyloid precursor protein) processing causes β-amyloid (Aβ) accumulation in autosomal dominant Alzheimer’s disease (AD), but it is unclear if it also affects sporadic Aβ accumulation. We tested healthy controls and patients with mild cognitive symptoms (N=331) in the BioFINDER study, using cerebrospinal fluid (CSF) Aβ40 as a surrogate for amyloidogenic APP processing.

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Early myo-inositol changes may precede Aβ pathology and relate to APOE genotype in Alzheimer disease

1 February, 2016

Background: We aimed to test whether in vivo levels of magnetic resonance spectroscopy (MRS) metabolites myo-inositol, N-acetyl-aspartate and choline are abnormal already during preclinical Alzheimer disease, relating these changes to amyloid and/or tau pathology, and functional connectivity. Methods: In this cross-sectional multi-center study (a subset of the prospective Swedish BioFINDER study) we included four groups,

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Total apolipoprotein E levels and specific isoform composition in cerebrospinal fluid and plasma from Alzheimer’s disease patients and controls.

27 January, 2016

The apolipoprotein E (ApoE) ε4 allele is the strongest risk factor of sporadic Alzheimer’s disease (AD), however, the fluid concentrations of ApoE and its different isoforms (ApoE2, ApoE3 and ApoE4) in AD patients and among APOE genotypes (APOE ε2, ε3, ε4) remain controversial. Using a novel mass spectrometry-based method, we quantified total ApoE and specific ApoE isoform concentrations and potential associations

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Flt3 ligand does not differentiate between Parkinsonian disorders.

BACKGROUND: Differential diagnosis of parkinsonian disorders is challenging because of overlapping symptoms, especially during early stages of disease. No validated biomarkers are available for early and accurate diagnosis of multiple system atrophy and other parkinsonian disorders. It has been reported that flt3 ligand levels in cerebrospinal fluid could clearly differentiate patients with Parkinson’s disease from

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Antibodies against phosphorylcholine are not altered in plasma of patients with Alzheimer’s disease

Background Phosphorylcholine is one of the major epitopes of oxidised low density lipoprotein. Low levels of IgM antibodies against phosphorylcholine (anti-PC) are associated with development of myocardial infarction and stroke. It has been shown that patients with Alzheimer’s disease and other dementias have significantly lower serum anti-PC levels compared to controls, suggesting that low levels

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Alzheimer’s disease cerebrospinal fluid biomarker in cognitively normal subjects.

In a large multicentre sample of cognitively normal subjects, as a function of age, gender and APOE genotype, we studied the frequency of abnormal cerebrospinal fluid levels of Alzheimer’s disease biomarkers including: total tau, phosphorylated tau and amyloid-β1-42. Fifteen cohorts from 12 different centres with either enzyme-linked immunosorbent assays or Luminex® measurements were selected for

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Disease-specific structural changes in thalamus and dentatorubrothalamic tract in progressive supranuclear palsy

INTRODUCTION: The aim of this study is to identify disease-specific changes of the thalamus, basal ganglia, pons, and midbrain in patients with progressive supranuclear palsy (PSP), Parkinson’s disease (PD), and multiple system atrophy with predominant parkinsonism (MSA-P) using diffusion tensor imaging and volumetric analysis. METHODS: MRI diffusion and volumetric data were acquired in a derivation

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Parkinson’s Disease Case Ascertainment in the EPIC Cohort: The NeuroEPIC4PD Study.

BACKGROUND: Large epidemiological prospective studies represent an important opportunity for investigating risk factors for rare diseases such as Parkinson’s disease (PD). Here we describe the procedures we used for ascertaining PD cases in the EPIC (European Prospective Investigation into Cancer and Nutrition) study. METHODS: The following three-phase procedure was used: (1) elaboration of a NeuroEPIC4PD

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Cerebral white matter lesions – associations with Aβ isoforms and amyloid PET

Small vessel disease (SVD) and amyloid deposition may promote each other, with a potential association between SVD and altered production or clearance of β-amyloid (Aβ) a ecting its cleavage products. We investigated the relationship between SVD, multiple isoforms of Aβ in cerebrospinal uid (CSF) and cortical Aβ in 831 subjects with cognitive performance ranging from

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Associations between TOMM40 Poly-T Repeat Variants and Dementia in Cases with Parkinsonism

BACKGROUND: Mitochondrial dysfunction has been implicated in the pathophysiology of Parkinson’s disease (PD)-related pathologies. OBJECTIVE: To investigate the role of the Translocase of the Outer Mitochondrial Membrane 40 homolog (TOMM40) variants in PD without dementia (PDND), PD with dementia (PDD) and in Dementia with Lewy bodies (DLB). METHODS: 248 individuals, including 92 PDND, 55 PDD,

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Cerebrospinal fluid neurogranin and YKL-40 as biomarkers of Alzheimer’s disease

OBJECTIVE: Widespread implementation of cerebrospinal fluid (CSF) biomarkers of Alzheimer’s disease (AD) in clinical settings requires improved accuracy for diagnosis of prodromal disease and for distinguishing AD from non-AD dementias. Novel and promising CSF biomarkers include neurogranin, a marker of synaptic degeneration, and YKL-40, a marker of neuroinflammation. METHODS: CSF neurogranin and YKL-40 were measured

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CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios improve the diagnostic accuracy for Alzheimer’s disease

11 December, 2015

New biomarkers of algorithms may improve the diagnostic accuracy of cerebrospinal fluid (CSF) for Alzheimer’s disease (AD. The present study aimed to determine whether Aβ42/Aβ40 and Aβ42/Aβ38 ratios improve the diagnostic accuracy of AD during predementia and dementia stages in comparison to CSF Aβ42 alone. The study included three different cohorts comprising a total of

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Increased cerebrospinal fluid biomarkers of angiogenesis in Parkinson’s disease.

20 July, 2015

Objective: To study biomarkers of angiogenesis in Parkinson’s disease (PD), and how these are associated with clinical characteristics, blood-brain barrier (BBB) permeability, and cerebrovascular disease. Methods: Thirty-eight elderly controls and 100 PD patients (82 without dementia and 18 with dementia) were included from the prospective Swedish BioFinder study. Cerebrospinal fluid (CSF) samples were analyzed for the

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Comparison of Amyloid PET and CSF Biomarkers for Identifying Early Alzheimer’s Disease

Objective To compare the diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers and amyloid PET for diagnosing early-stage Alzheimer’s disease (AD). Methods From the BioFINDER study, we included 122 healthy elderly and 34 patients with mild cognitive impairment who developed AD dementia within 3 years (MCI-AD). Amyloid-β (Aβ) in 8 brain regions and globally was examined

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Comparison of Amyloid PET and CSF Biomarkers for Identifying Early Alzheimer’s Disease.

13 June, 2015

Neurology. 2015 Oct 6;85(14):1240-9.

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Increased cerebrospinal fluid biomarkers of angiogenesis in Parkinson’s disease.

Neurology, 2015 Nov 24;85(21):1834-42.

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Longitudinal cerebrospinal fluid biomarker measurements in preclinical sporadic Alzheimer’s disease: A prospective 9-year study.

Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring. 2015 1: 4, 403–411.

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Cerebrospinal fluid levels of IL-6 are decreased and correlate with cognitive status in DLB patients

Alzheimer’s Research & Therapy. 2015 Oct 5;7(1):63.

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Extrapolation-Based References Improve Motion and Eddy-Current Correction of High B-Value DWI Data: Application in Parkinson’s Disease Dementia.

PLoS One. 2015 Nov 3;10(11):e0141825

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Antibodies against phosphorylcholine are not altered in plasma of patients with Alzheimer’s disease.

BMC Neurol 2015, 15:8.

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Alzheimer’s disease cerebrospinal fluid biomarker in cognitively normal subjects.

Alzheimer’s Disease Neuroimaging Initiative. Brain. 2015 Sep;138(Pt 9):2701-15.

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Disease-specific structural changes in thalamus and dentatorubrothalamic tract in progressive supranuclear palsy.

Neuroradiology. 2015 Nov;57(11):1079-91.

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Parkinson’s Disease Case Ascertainment in the EPIC Cohort: The NeuroEPIC4PD Study.

Neurodegener Dis. 2015;15(6):331-8.

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Associations between TOMM40 Poly-T Repeat Variants and Dementia in Cases with Parkinsonism.

Ann Clin Transl Neurol. 2015 Nov 20;3(1):12-20.

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Cerebrospinal fluid neurogranin and YKL-40 as biomarkers of Alzheimer’s disease. 

Ann Clin Transl Neurol. 2015 Nov 20;3(1):12-20.

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Cerebral Microbleeds and White Matter Hyperintensities in Cognitively Healthy Elderly: A Cross-sectional Cohort Study Evaluating the Effect of Arterial Stiffness.

Cerebrovascular Diseases EXTRA, 2015;5:41–51.

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CSF biomarkers and clinical progression of Parkinson disease.

Neurology, 2015 Jan 6;84(1):57-63.

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Cerebral Microbleeds and White Matter Hyperintensities in Cognitively Healthy Elderly: A Cross-sectional Cohort Study Evaluating the Effect of Arterial Stiffness

19 March, 2015

Background: Arterial stiffness reflects the ageing processes in the vascular system and studies have shown an association between reduced cognitive function and cerebral small vessel disease. Small vessel disease can be visualized as white matter hyperintensities (WMH) and lacunar infarcts but also as cerebral microbleeds on brain magnetic resonance imaging (MRI). We aimed to investigate

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CSF biomarkers and clinical progression of Parkinson disease

23 January, 2015

Objective: To investigate whether certain CSF biomarkers at baseline can predict future progression of motor symptoms and cognitive decline in patients with Parkinson disease (PD). Methods: Patients and controls were recruited from hospitals in southern Sweden as part of the prospective and longitudinal Swedish BioFinder Study. In the present study, we included 42 patients with

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Apolipoprotein E genotype and the diagnostic accuracy of cerebrospinal fluid biomarkers for Alzheimer disease

1 October, 2014

IMPORTANCE: Several studies suggest that the apolipoprotein E (APOE) epsilon4 allele modulates cerebrospinal fluid (CSF) levels of beta-amyloid 42 (Abeta42). Whether this effect is secondary to the association of the APOE epsilon4 allele with cortical Abeta deposition or whether APOE epsilon4 directly influences CSF levels of Abeta42 independently of Abeta pathology remains unknown. OBJECTIVE: To

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Accuracy of Brain Amyloid Detection in Clinical Practice Using Cerebrospinal Fluid beta-Amyloid 42

13 June, 2014

JAMA Neurol. 2014 Oct;71(10):1282-9.

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Apolipoprotein E genotype and the diagnostic accuracy of cerebrospinal fluid biomarkers for Alzheimer disease.

Alzheimer’s Disease Neuroimaging Initiative. JAMA Psychiatry. 2014;71(10):1183-91.

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Levels of cerebrospinal fluid alpha-synuclein oligomers are increased in Parkinson’s disease with dementia and dementia with Lewy bodies compared to Alzheimer’s disease

7 May, 2014

INTRODUCTION: The objective was to study whether alpha-synuclein oligomers are altered in the cerebrospinal fluid (CSF) of patients with dementia, including Parkinson disease with dementia (PDD), dementia with Lewy bodies (DLB), and Alzheimer disease (AD), compared with age-matched controls. METHODS: In total, 247 CSF samples were assessed in this study, including 71 patients with DLB,

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Low levels of soluble NG2 in cerebrospinal fluid from patients with dementia with Lewy bodies

21 January, 2014

The proteoglycan NG2 plays a major role in proliferation, migration, and differentiation of pericytes and NG2 cells in the brain. We have previously reported decreased soluble NG2 (sNG2) levels in cerebrospinal fluid (CSF) from patients with Alzheimer’s disease (AD) and a relationship between sNG2 and AD biomarkers in these patients. To further investigate whether alterations

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Cerebrospinal fluid inflammatory markers in Parkinson’s disease–associations with depression, fatigue, and cognitive impairment

31 July, 2013

Neuroinflammation may be involved in the pathophysiology of Parkinson’s disease (PD) and specifically in non-motor symptoms such as depression, fatigue and cognitive impairment. The aim of this study was to measure inflammatory markers in cerebrospinal fluid (CSF) samples from PD patients and a reference group, and to investigate correlations between non-motor symptoms and inflammation. We

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Abeta1-15/16 as a potential diagnostic marker in neurodegenerative diseases

13 June, 2013

Neuromolecular Medicine. 2013;15(1):169-79.

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Assessment of global and regional diffusion changes along white matter tracts in parkinsonian disorders by MR tractography

PURPOSE: The aim of the study was to determine the usefulness of diffusion tensor tractography (DTT) in parkinsonian disorders using a recently developed method for normalization of diffusion data and tract size along white matter tracts. Furthermore, the use of DTT in selected white matter tracts for differential diagnosis was assessed. METHODS: We quantified global

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Low CSF levels of both alpha-synuclein and the alpha-synuclein cleaving enzyme neurosin in patients with synucleinopathy

8 January, 2013

Neurosin is a protease that in vitro degrades alpha-synuclein, the main constituent of Lewy bodies found in brains of patients with synucleinopathy including Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). Several studies have reported reduced cerebrospinal fluid (CSF) levels of alpha-synuclein in synucleinopathy patients and recent data also proposes a significant role of

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Abeta1-15/16 as a potential diagnostic marker in neurodegenerative diseases

7 December, 2012

Cerebrospinal fluid (CSF) biomarkers for Alzheimer’s disease (AD) reflect brain biochemistry. Using combined immunoprecipitation and mass spectrometry, we have shown that amyloid beta 1-15 (Abeta1-15) is produced by concerted beta- and alpha-secretase cleavage of amyloid precursor protein (APP) and that the relative levels of Abeta1-16 in AD compared to controls are increased. Furthermore, drug-induced gamma-secretase

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