Performance of αSynuclein RT-QuIC in relation to neuropathological staging of Lewy body disease.

17 June, 2022

Acta Neuropathol Commun. 2022 Jun 22;10(1):90. doi: 10.1186/s40478-022-01388-7.

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Astrocytic function is associated with both amyloid-β and tau pathology in non-demented APOE ϵ4 carriers.

Brain Commun. 2022 May 22;4(3):fcac135. doi: 10.1093/braincomms/fcac135.

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Test-retest variability of plasma biomarkers in Alzheimer’s disease and its effects on clinical prediction models.

Alzheimers Dement. 2022 Jun 14:10.1002/alz.12706. doi: 10.1002/alz.12706.

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β-Amyloid-Dependent and -Independent Genetic Pathways Regulating CSF Tau Biomarkers in Alzheimer Disease.

Neurology. 2022 May 31;99(5):e476-87. doi: 10.1212/WNL.0000000000200605.

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Diagnostic and prognostic performance to detect Alzheimer’s disease and clinical progression of a novel assay for plasma p-tau217.

Alzheimers Res Ther. 2022 May 14;14(1):67. doi: 10.1186/s13195-022-01005-8.

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Combining plasma phospho-tau and accessible measures to evaluate progression to Alzheimer’s dementia in mild cognitive impairment patients.

Alzheimers Res Ther. 2022 Mar 29;14(1):46. doi: 10.1186/s13195-022-00990-0.

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Development of Apathy, Anxiety, and Depression in Cognitively Unimpaired Older Adults: Effects of Alzheimer’s Disease Pathology and Cognitive Decline.

Biol Psychiatry. 2022 Jan 31:S0006-3223(22)00053-1. doi: 10.1016/j.biopsych.2022.01.012.

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Midsagittal corpus callosal thickness and cognitive impairment in Parkinson’s disease.

Eur J Neurosci. 2022 Apr;55(7):1859-1872. doi: 10.1111/ejn.15640.

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Subtypes of Alzheimer’s disease: questions, controversy, and meaning.

Trends Neurosci. 2022 May;45(5):342-345. doi: 10.1016/j.tins.2022.02.001.

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Cerebrospinal Fluid Biomarkers in Autopsy-Confirmed Alzheimer Disease and Frontotemporal Lobar Degeneration.

Neurology. 2022 Mar 15;98(11):e1137-e1150. doi: 10.1212/WNL.0000000000200040.

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The Neuroinflammatory Acute Phase Response in Parkinsonian-Related Disorders.

Mov Disord. 2022 Feb 8. doi: 10.1002/mds.28958.

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Cerebrospinal fluid neurofilament light chain differentiates primary psychiatric disorders from rapidly progressive, Alzheimer’s disease and frontotemporal disorders in clinical settings.

Alzheimers Dement. 2022 Feb 1. doi: 10.1002/alz.12549.

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Components of gait in people with and without mild cognitive impairment.

Gait Posture. 2022 Mar;93:83-89. doi: 10.1016/j.gaitpost.2022.01.012.

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Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum.

JAMA Neurol. 2022 Mar 1;79(3):228-243. doi: 10.1001/jamaneurol.2021.5216.

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Biomarker-Based Prediction of Longitudinal Tau Positron Emission Tomography in Alzheimer Disease.

JAMA Neurol. 2022 Feb 1;79(2):149-158. doi: 10.1001/jamaneurol.2021.4654.

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Blood-based biomarkers for Alzheimer’s disease.

EMBO Mol Med. 2022 Jan 11;14(1):e14408. doi: 10.15252/emmm.202114408.

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Blood-based biomarkers for Alzheimer’s disease: towards clinical implementation.

Lancet Neurol. 2022 Jan;21(1):66-77. doi: 10.1016/S1474-4422(21)00361-6.

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Serum Neurofilament Light Chain as a Marker of Progression in Parkinson’s Disease: Long-Term Observation and Implications of Clinical Subtypes.

J Parkinsons Dis. 2022;12(2):571-584. doi: 10.3233/JPD-212866.

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Connecting Cohorts to Diminish Alzheimer’s Disease (CONCORD-AD): A Report of an International Research Collaboration Network.

J Alzheimers Dis. 2022;85(1):31-45. doi: 10.3233/JAD-210525.

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Insights on Genetic and Environmental Factors in Parkinson’s Disease from a Regional Swedish Case-Control Cohort.

J Parkinsons Dis. 2022;12(1):153-171. doi: 10.3233/JPD-212818.

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Detecting amyloid positivity in early Alzheimer’s disease using combinations of plasma Aβ42/Aβ40 and p-tau.

Alzheimers Dement. 2022 Feb;18(2):283-293. doi: 10.1002/alz.12395.

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Decreased pain sensitivity and alterations of cerebrospinal fluid and plasma inflammatory mediators after total hip arthroplasty in patients with disabling osteoarthritis.

Pain Pract. 2022 Jan;22(1):66-82. doi: 10.1111/papr.13051.

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The BIN1 rs744373 Alzheimer’s disease risk SNP is associated with faster Aβ-associated tau accumulation and cognitive decline.

Alzheimers Dement. 2022 Jan;18(1):103-115. doi: 10.1002/alz.12371.

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Prenatal Gyrification Pattern Affects Age at Onset in Frontotemporal Dementia.

Santillo A.Cereb Cortex. 2022 Jan 17:bhab457. doi: 10.1093/cercor/bhab457.

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Association of β-Amyloid Accumulation With Executive Function in Adults With Unimpaired Cognition.

Alzheimer’s Disease Neuroimaging Initiative.Neurology. 2022 Jan 12:10.1212/WNL.0000000000013299. doi: 10.1212/WNL.0000000000013299.

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Cellular localization of p-tau217 in brain and its association with p-tau217 plasma levels.

Acta Neuropathol Commun. 2022 Jan 6;10(1):3. doi: 10.1186/s40478-021-01307-2.

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Cerebrospinal fluid N-224 tau helps discriminate Alzheimer’s disease from subjective cognitive decline and other dementias.

3 February, 2022

Abstract Background: Elevated cerebrospinal fluid (CSF) concentrations of total tau (T-tau) and phosphorylated tau at Thr181 (P-tau181) protein are typical of Alzheimer’s disease (AD). However, the T-tau assay measures only the mid-region of the protein, while tau in CSF is instead composed of a series of fragments. One fragment species in particular, N-224, shows increased levels

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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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Association of CSF Aβ38 Levels With Risk of Alzheimer Disease-Related Decline.

14 June, 2021

Neurology. 2021 Dec 22:10.1212/WNL.0000000000013228. doi: 10.1212/WNL.0000000000013228. PMID: 34937781

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Biomarker-Based Prediction of Longitudinal Tau Positron Emission Tomography in Alzheimer Disease.

JAMA Neurol. 2021 Dec 20:e214654. doi: 10.1001/jamaneurol.2021.4654..PMID: 34928318 Free PMC article.

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Validation of Plasma Amyloid-β 42/40 for Detecting Alzheimer Disease Amyloid Plaques.

Neurology. 2021 Dec 14:10.1212/WNL.0000000000013211. doi: 10.1212/WNL.0000000000013211..PMID: 34906975

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The protective gene dose effect of the APOE ε2 allele on gray matter volume in cognitively unimpaired individuals.

ALFA study†, BioFINDER, ADNI.Alzheimers Dement. 2021 Dec 8. doi: 10.1002/alz.12487.

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Characterization of pre-analytical sample handling effects on a panel of Alzheimer’s disease-related blood-based biomarkers: Results from the Standardization of Alzheimer’s Blood Biomarkers (SABB) working group.

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Connecting Cohorts to Diminish Alzheimer’s Disease (CONCORD-AD): A Report of an International Research Collaboration Network.

CONCORD-AD investigators.J Alzheimers Dis. 2022;85(1):31-45. doi: 10.3233/JAD-210525.

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The global Alzheimer’s Association round robin study on plasma amyloid β methods.

Alzheimers Dement (Amst). 2021 Oct 14;13(1):e12242. doi: 10.1002/dad2.12242. eCollection 2021.

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Genetic effects on longitudinal cognitive decline during the early stages of Alzheimer’s disease.

Sci Rep. 2021 Oct 6;11(1):19853. doi: 10.1038/s41598-021-99310-z.

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Head-to-Head Comparison of 8 Plasma Amyloid-β 42/40 Assays in Alzheimer Disease.

JAMA Neurol. 2021 Nov 1;78(11):1375-1382. doi: 10.1001/jamaneurol.2021.3180.

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Comparing the Clinical Utility and Diagnostic Performance of CSF P-Tau181, P-Tau217, and P-Tau231 Assays.

Neurology. 2021 Oct 26;97(17):e1681-e1694. doi: 10.1212/WNL.0000000000012727. Epub 2021 Sep 7.

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Plasma phosphorylated tau 217 and phosphorylated tau 181 as biomarkers in Alzheimer’s disease and frontotemporal lobar degeneration: a retrospective diagnostic performance study.

Advancing Research and Treatment for Frontotemporal Lobar Degeneration investigators.Lancet Neurol. 2021 Sep;20(9):739-752. doi: 10.1016/S1474-4422(21)00214-3.

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Tau-related grey matter network breakdown across the Alzheimer’s disease continuum.

Alzheimers Res Ther. 2021 Aug 13;13(1):138. doi: 10.1186/s13195-021-00876-7.

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Inter-modality assessment of medial temporal lobe atrophy in a non-demented population: application of a visual rating scale template across radiologists with varying clinical experience.

Eur Radiol. 2022 Feb;32(2):1127-1134. doi: 10.1007/s00330-021-08177-1. Epub 2021 Jul 30.

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Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer’s disease.

Brain. 2021 Dec 16;144(11):3505-3516. doi: 10.1093/brain/awab223.

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Tau PET correlates with different Alzheimer’s disease-related features compared to CSF and plasma p-tau biomarkers.

EMBO Mol Med. 2021 Aug 9;13(8):e14398. doi: 10.15252/emmm.202114398. Epub 2021 Jul 13.

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Accuracy of Tau Positron Emission Tomography as a Prognostic Marker in Preclinical and Prodromal Alzheimer Disease: A Head-to-Head Comparison Against Amyloid Positron Emission Tomography and Magnetic Resonance Imaging.

JAMA Neurol. 2021 Aug 1;78(8):961-971. doi: 10.1001/jamaneurol.2021.1858.

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Detecting amyloid positivity in early Alzheimer’s disease using combinations of plasma Aβ42/Aβ40 and p-tau.

Alzheimers Dement. 2021 Jun 20. doi: 10.1002/alz.12395.

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Plasma biomarkers of Alzheimer’s disease improve prediction of cognitive decline in cognitively unimpaired elderly populations.

Nat Commun. 2021 Jun 11;12(1):3555. doi: 10.1038/s41467-021-23746-0.

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A multicentre validation study of the diagnostic value of plasma neurofilament light.

Nat Commun. 2021 Jun 7;12(1):3400. doi: 10.1038/s41467-021-23620-z.

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Sex differences in off-target binding using tau positron emission tomography.

Neuroimage Clin. 2021;31:102708. doi: 10.1016/j.nicl.2021.102708. Epub 2021 May 29.

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Plasma markers predict changes in amyloid, tau, atrophy and cognition in non-demented subjects.

Brain. 2021 Oct 22;144(9):2826-2836. doi: 10.1093/brain/awab163.

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The BIN1 rs744373 Alzheimer’s disease risk SNP is associated with faster Aβ-associated tau accumulation and cognitive decline.

Alzheimer’s Disease Neuroimaging Initiative (ADNI)* and the Swedish BioFINDER study.Alzheimers Dement. 2021 Jun 1. doi: 10.1002/alz.12371. Online ahead of print.

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A multicenter comparison of [18F]flortaucipir, [18F]RO948, and [18F]MK6240 tau PET tracers to detect a common target ROI for differential diagnosis.

Eur J Nucl Med Mol Imaging. 2021 Jul;48(7):2295-2305. doi: 10.1007/s00259-021-05401-4. Epub 2021 May 27.

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Health utility in preclinical and prodromal Alzheimer’s disease for establishing the value of new disease-modifying treatments-EQ-5D data from the Swedish BioFINDER study.

Alzheimers Dement. 2021 Nov;17(11):1832-1842. doi: 10.1002/alz.12355. Epub 2021 May 13.

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Soluble P-tau217 reflects amyloid and tau pathology and mediates the association of amyloid with tau.

EMBO Mol Med. 2021 Jun 7;13(6):e14022. doi: 10.15252/emmm.202114022. Epub 2021 May 5.PMID: 33949133 Free PMC article.

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Four distinct trajectories of tau deposition identified in Alzheimer’s disease.

Nat Med. 2021 May;27(5):871-881. doi: 10.1038/s41591-021-01309-6. Epub 2021 Apr 29.

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Cerebrospinal fluid N-224 tau helps discriminate Alzheimer’s disease from subjective cognitive decline and other dementias.

Alzheimers Res Ther. 2021 Feb 8;13(1):38. doi: 10.1186/s13195-020-00756-6.

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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.

Nat Med. 2020 Mar;26(3):379-386

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Accelerated inflammatory aging in Alzheimer’s disease and its relation to amyloid,
tau, and cognition.

Sci Rep. 2021
Jan 21;11(1):1965.

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The diagnostic and prognostic capabilities of plasma biomarkers in Alzheimer’s
disease.

Alzheimers Dement. 2021 Jan 25. Online ahead of print.

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Mild behavioral impairment and its relation to tau pathology in preclinical Alzheimer’s
disease.

Transl Psychiatry.
2021 Jan 26;11(1):76.

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Neuroligin-1 in brain and CSF of neurodegenerative disorders: investigation for
synaptic biomarkers.

Acta Neuropathol Commun. 2021 Feb 1;9(1):19.

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Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future
conversion to Alzheimer dementia in patients with mild cognitive impairment.

Alzheimers Res Ther. 2021 Mar 27;13(1):68.

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A multisite analysis of the concordance between visual image interpretation and
quantitative analysis of [18F]flutemetamol amyloid PET images.

Eur J Nucl Med Mol Imaging. 2021 Jul;48(7):2183-2199

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Heterogeneous distribution of tau pathology in the behavioural variant of Alzheimer’s
disease.

J Neurol Neurosurg Psychiatry. 2021 Apr 13:jnnp-2020-325497.

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Biomarker testing in MCI patients-deciding who to test.

Alzheimers Res Ther. 2021 Jan 7;13(1):14.

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Comparing ATN-T designation by tau PET visual reads, tau PET quantification, and CSF PTau181 across three cohorts.

Alzheimer’s Disease Neuroimaging Initiative (ADNI).Eur J Nucl Med Mol Imaging. 2021 Jul;48(7):2259-2271

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

14 June, 2020

Neurology. 2021 Jan 12;96(2):e193-e202.

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Plasma Phospho-Tau Identifies Alzheimer’s Co-Pathology in Patients with Lewy Body Disease.

Mov Disord. 2021 Mar;36(3):767-771

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Evaluation of a novel immunoassay to detect p-tau Thr217 in the CSF to distinguish Alzheimer disease from other dementias.

Neurology. 2020 Dec 1;95(22):e3026-e3035.

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Patient-centered connectivity-based prediction of tau pathology spread in Alzheimer’s disease.

Sci Adv. 2020 Nov 27;6(48)

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Plasma NT1 Tau is a Specific and Early Marker of Alzheimer’s Disease.

Ann Neurol. 2020 Nov;88(5):878-892.

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Blood and cerebrospinal fluid neurofilament light differentially detect neurodegeneration in early Alzheimer’s disease.

Neurobiol Aging. 2020 Nov;95:143-153.

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The impact of demographic, clinical, genetic, and imaging variables on tau PET status.

Eur J Nucl Med Mol Imaging. 2020 Nov 19.2021 Jul;48(7):2245-2258

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Acute phase markers in CSF reveal inflammatory changes in Alzheimer’s disease that intersect with pathology, APOE ε4, sex and age.

Prog Neurobiol. 2020 Aug 31:101904.

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Image reconstruction methods affect software-aided assessment of pathologies of [18F]flutemetamol and [18F]FDG brain-PET examinations in patients with neurodegenerative diseases.

Neuroimage Clin. 2020;28:102386.

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Validation of a spatial normalization method using a principal component derived adaptive template for [18F]florbetaben PET.

Am J Nucl Med Mol Imaging. 2020 Aug 25;10(4):161-167. eCollection 2020.

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Medial temporal atrophy in preclinical dementia: Visual and automated assessment during six year follow-up.

Neuroimage Clin. 2020 Jun 10;27:102310.

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The effects of tau, amyloid and white matter lesions on mobility, dual tasking and balance in older people.

J Gerontol A Biol Sci Med Sci. 2020 Jun 7:glaa143.

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Spread of pathological tau proteins through communicating neurons in human Alzheimer’s disease.

Nat Commun. 2020 May 26;11(1):2612.

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Biomarker profiling beyond amyloid and tau: cerebrospinal fluid markers, hippocampal atrophy, and memory change in cognitively unimpaired older adults.

Neurobiol Aging. 2020 Sep;93:1-15.

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CDH6 and HAGH protein levels in plasma associate with Alzheimer’s disease in APOE ε4 carriers.

Sci Rep. 2020 May 19;10(1):8233.

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Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer’s disease

Sci Adv. 2020 Apr 15;6(16):eaaz2387.

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The implications of different approaches to define AT(N) in Alzheimer disease.

Neurology. 2020 May 26;94(21):e2233-e2244

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Diagnostic Performance of RO948 F 18 Tau Positron Emission Tomography in the Differentiation of Alzheimer Disease From Other Neurodegenerative Disorders.

JAMA Neurol. 2020 May 11:e200989.

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Blood phosphorylated tau 181 as a biomarker for Alzheimer’s disease: a diagnostic performance and prediction modelling study using data from four prospective cohorts.

Lancet Neurol. 2020 May;19(5):422-433.

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Relationship between cortical iron and tau aggregation in Alzheimer’s disease.

Brain. 2020 May 1;143(5):1341-1349.

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Medial temporal lobe connectivity and its associations with cognition in early Alzheimer’s disease.

Brain. 2020 Apr 1;143(4):1233-1248.

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Cerebrospinal fluid p-tau217 performs better than p-tau181 as a biomarker of Alzheimer’s disease.

Nat Commun. 2020 Apr 3;11(1):1683.

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The age-related effect on cognitive performance in cognitively healthy elderly is mainly caused by underlying AD pathology or cerebrovascular lesions: implications for cutoffs regarding cognitive impairment.

Alzheimers Res Ther. 2020 Mar 24;12(1):30.

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Towards unconstrained compartment modeling in white matter using diffusion-relaxation MRI with tensor-valued diffusion encoding.

Reson Med. 2020 Sep;84(3):1605-1623.

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Longitudinal degeneration of the basal forebrain predicts subsequent dementia in Parkinson’s disease.

Neurobiol Dis. 2020 Mar 4, 2020-06-01, Volume 139, Article 104831

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[18F]Flortaucipir Distinguishes Alzheimer’s disease from progressive supranuclear palsy pathology in a mixed-pathology case.

Acta Neuropathol 2020 Feb;139(2):411-413.

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Cerebrospinal fluid neurogranin in an inducible mouse model of neurodegeneration: A translatable marker of synaptic degeneration. 

Neurobiol Dis. 2020 Feb;134:104645.

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Head-to-head comparison of tau positron emission tomography tracers  [18F]flortaucipir and [18F]RO948.

Eur J Nucl Med Mol Imaging. 2020 Feb;47(2):342-354.

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Apathy and anxiety are early markers of Alzheimer’s disease.

Neurobiol Aging. 2020 Jan;85:74-82.

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Functional brain architecture is associated with the rate of tau accumulation in Alzheimer’s disease.

Alzheimer’s Disease Neuroimaging Initiative (ADNI). Nat Commun. 2020 Jan 17;11(1):347.

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Cognitively normal women with Alzheimer’s disease proteinopathy show relative preservation of memory but not of hippocampal volume.

13 June, 2019

Alzheimers Res Ther. 2019 Dec 26;11(1):109.

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Cerebrospinal fluid levels of neurogranin in Parkinsonian disorders.

Mov Disord. 2020 Mar;35(3):513-518.

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Diffusion Tensor MRI to Distinguish Progressive Supranuclear Palsy from α-Synucleinopathies. 

Radiology. 2019 Dec;293(3):646-653.

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Amyloid and tau accumulate across distinct spatial networks and are differentially associated with brain connectivity.

Elife. 2019 Dec 9;8:e50830.

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Predicting Clinical decline and conversion to Alzheimer’s disease or dementia using novel Elecsys Aβ(1-42), pTau and tTau CSF immunoassays

Sci Rep. 2019 Dec 13;9(1):19024.

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Cerebrospinal fluid and plasma biomarker trajectories with increasing amyloid deposition in Alzheimer’s disease.

EMBO Mol Med. 2019 Dec;11(12):e11170.

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Multiplex proteomics identifies novel CSF and plasma biomarkers of early Alzheimer’s disease. 

Acta Neuropathol Commun. 2019 Nov 6;7(1):169.

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A quick test of cognitive speed can predict development of dementia in Parkinson’s disease. 

Sci Rep. 2019 Oct 28;9(1):15417.

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Autocatalytic amplification of Alzheimer-associated Aβ42 peptide aggregation in human cerebrospinal fluid.

Commun Biol. 2019 Oct 8;2:365.

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Alzheimer’s Disease Neuroimaging Initiative. Biomarker-based prognosis for people with mild cognitive impairment (ABIDE): a modelling study.

Lancet Neurol. 2019 Nov;18(11):1034-1044

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Endo-lysosomal proteins and ubiquitin CSF concentrations in Alzheimer’s and Parkinson’s disease. 

Alzheimers Res Ther. 2019 Sep 14;11(1):82

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Increased functional connectivity of thalamic subdivisions in patients with Parkinson’s disease.

PLoS One. 2019 Sep 4;14(9):e0222002.

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β-amyloid pathology and hippocampal atrophy are independently associated with memory function in cognitively healthy elderly. 

Sci Rep. 2019 Aug 1;9(1):11180.

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α-synuclein-lipoprotein interactions and elevated ApoE level in cerebrospinal fluid from Parkinson’s disease patients.  

Proc Natl Acad Sci U S A. 2019 Jul 23;116(30):15226-15235.

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Determining clinically meaningful decline in preclinical Alzheimer disease.

Neurology. 2019 Jul 23;93(4):e322-e333.

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Towards a unified protocol for handling of CSF before β-amyloid measurements. 

Alzheimers Res Ther. 2019 Jul 19;11(1):63.

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Staging β-Amyloid Pathology With Amyloid Positron Emission Tomography. 

JAMA Neurol. 2019 Jul 17;76(11)

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Low prevalence of known pathogenic mutations in dominant PD genes: A Swedish multicenter study.

Parkinsonism Relat Disord. 2019 Sep 6.

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European Ultrahigh-Field Imaging Network for Neurodegenerative Diseases (EUFIND). 

Alzheimers Dement (Amst). 2019 Jul 31;11:538-549.

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Performance of Fully Automated Plasma Assays as Screening Tests for Alzheimer Disease-Related β-Amyloid Status. 

JAMA Neurol. 2019 Sep; 76(9): 1060–1069

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Levels of islet amyloid polypeptide in cerebrospinal fluid and plasma from patients with Alzheimer’s disease. 

PLoS One. 2019 Jun 17;14(6):e0218561.

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Mapping of apparent susceptibility yields promising diagnostic separation of progressive supranuclear palsy from other causes of parkinsonism. 

Sci Rep. 2019 Apr 15;9(1):6079.

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Association Between Earliest Amyloid Uptake and Functional Connectivity in Cognitively Unimpaired Elderly. 

Cereb Cortex. 2019 May 1;29(5):2173-2182

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Searching for the neurite density with diffusion MRI: Challenges for biophysical modeling. 

Hum Brain Mapp. 2019 Jun 1;40(8):2529-2545.

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Structural imaging findings on non-enhanced computed tomography are severely underreported in the primary care diagnostic work-up of subjective cognitive decline.

Neuroradiology. 2019 Apr;61(4):397-404.

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Cerebrospinal Fluid Concentrations of Extracellular Matrix Proteins in Alzheimer’s Disease. 

J Alzheimers Dis. 2019;69(4):1213-1220

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CSF placental growth factor – a novel candidate biomarker of frontotemporal dementia. 

Ann Clin Transl Neurol. 2019 Mar 29;6(5):863-872.

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Accurate risk estimation of β-amyloid positivity to identify prodromal Alzheimer’s disease: Cross-validation study of practical algorithms. 

Alzheimers Dement. 2019 Feb;15(2):194-204.

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Association of IL1RAP-related genetic variation with cerebrospinal fluid concentration of Alzheimer-associated tau protein. 

Sci Rep. 2019 Feb 21;9(1):2460.

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Data-driven approaches for tau-PET imaging biomarkers in Alzheimer’s disease.

Hum Brain Mapp. 2019 Feb 1;40(2):638-651.

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Predicting diagnosis and cognition with 18F-AV-1451 tau PET and structural MRI in Alzheimer’s disease. 

Alzheimers Dement. 2019 Apr;15(4):570-580.

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Associations between tau, Aβ, and cortical thickness with cognition in Alzheimer disease. 

Neurology. 2019 Feb 5;92(6):e601-e612.

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Brain myoinositol as a potential marker of amyloid-related pathology: A longitudinal study. 

Neurology. 2019 Jan 29; 92(5): e395–e405

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Novel tau fragments in cerebrospinal fluid: relation to tangle pathology and cognitive decline in Alzheimer’s disease. 

Acta Neuropathol. 2019 Feb;137(2):279-296.

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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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Correlation of In Vivo [18F]Flortaucipir With Postmortem Alzheimer Disease Tau Pathology.

13 June, 2018

JAMA Neurol. 2019 Mar; 76(3): 310–31

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Exploring causality of the association between smoking and Parkinson’s disease.

Int J Epidemiol. 2019 Jun; 48(3): 912–925.

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Effects of APOE ε4 on neuroimaging, cerebrospinal fluid biomarkers, and cognition in prodromal Alzheimer’s disease.

Neurobiol Aging. 2018 Nov;71:81-90.

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Prevalence of amyloid-β pathology in distinct variants of primary progressive aphasia.  

Ann Neurol. 2018 Nov;84(5):729-740.

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Parkinson’s disease: evolution of cognitive impairment and CSF Aβ1-42 profiles in a prospective longitudinal study.  

J Neurol Neurosurg Psychiatry. 2019 Feb;90(2):165-170.

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Cerebrospinal fluid concentrations of inflammatory markers in Parkinson’s disease and atypical parkinsonian disorders.

Sci Rep. 2018 Sep 5;8(1):13276.

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Greater tau load and reduced cortical thickness in APOE ε4-negative Alzheimer’s disease: a cohort study. 

Alzheimers Res Ther. 2018 Aug 7;10(1):77.

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Regional times to equilibria and their impact on semi-quantification of [18F]AV-1451 uptake.

J Cereb Blood Flow Metab. 2018 Aug 3:271678X18791430.

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The impact of preanalytical variables on measuring cerebrospinal fluid biomarkers for Alzheimer’s disease diagnosis: A Review.  

Alzheimers Dement. 2018-10-01, Volume 14, Issue 10, Pages 1313-133.

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Is longitudinal tau PET ready for use in Alzheimer’s disease clinical trials?

Brain. 2018 May 1;141(5):1241-1244.

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Slowly progressive dementia caused by MAPT R406W mutations: longitudinal report on a new kindred and systematic Review.

Alzheimers Res Ther. 2018 Jan 9;10(1):2.

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Alzheimer’s Disease Neuroimaging Initiative. Amyloid pathology in the progression to mild cognitive impairment.

Neurobiol Aging. 2018 Apr;64:76-84.

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Altered structural network organization in cognitively normal individuals with amyloid pathology. 

Neurobiol Aging. 2018 Apr;64:15-24.

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Association of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia.

JAMA   Psychiatry. 2018 Jan 1;75(1):84-95.

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Amyloid Network Topology Characterizes the Progression of Alzheimer’s Disease During the Predementia Stages.

Alzheimer’s Disease Neuroimaging Initiative. Cereb Cortex. 2018 Jan 1;28(1):340-349.

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Amyloid blood biomarker detects Alzheimer’s disease.

EMBO Mol Med. 2018 May;10(5). pii:e8763.

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Prevalence of the apolipoprotein E ε4 allele in amyloid β positive subjects across the spectrum of Alzheimer’s disease.

Alzheimers Dement. 2018-07-01, Volume 14, Issue 7, Pages 913-92

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Striatal changes in Parkinson disease: An investigation of morphology, functional connectivity and their relationship to clinical symptoms.

Psychiatry Res. 2018 May 30;275:5-13

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18F-AV-1451 in Parkinson’s Disease with and without dementia and in Dementia with Lewy Bodies.  

Sci Rep. 2018 Mar 16;8(1):4717.

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Assessment of kallikrein 6 as a cross-sectional and longitudinal biomarker for Alzheimer’s disease. 

Alzheimers Res Ther. 2018 Jan 29;10(1):9.

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Alteration of putaminal fractional anisotropy in Parkinson’s disease: a longitudinal diffusion kurtosis imaging study. 

Neuroradiology. 2018  Mar;60(3):247-254.

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

25 August, 2017

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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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Abnormal Structural Brain Connectome in Individuals with Preclinical Alzheimer’s Disease.

13 June, 2017

Hansson O. Cereb Cortex. 2017 Oct 3:1-12.

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The effect of white matter hyperintensities on statistical analysis of diffusion tensor imaging in cognitively healthy elderly and prodromal Alzheimer’s disease.

PLoS One. 2017 Sep 21;12(9):e0185239.  eCollection 2017.

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A novel quantification-driven proteomic strategy identifies an endogenous peptide of pleiotrophin as a new biomarker of Alzheimer’s disease. 

Sci Rep. 2017 Oct 17;7(1):13333.

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CSF/serum albumin ratio in dementias: a cross-sectional study on 1861 patients.

Neurobiol Aging. 2017 Nov;59:1-9.

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Preclinical effects of APOE ε4 on cerebrospinal fluid Aβ42 concentrations. 

Alzheimers Res Ther. 2017 Oct 23;9(1):87.

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Mass Spectrometric Analysis of Cerebrospinal Fluid Ubiquitin in Alzheimer’s Disease and Parkinsonian Disorders. 

Proteomics Clin Appl. 2017  Dec;11(11-12).

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Association between cerebrospinal fluid and plasma neurodegeneration biomarkers with brain atrophy in Alzheimer’s disease. 

Alzheimer’s Disease Neuroimaging Initiative. Neurobiol Aging. 2017 Oct;58:14-29.

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

Nature communications. 2017 Oct 31;8(1):1214.

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Concordance between different amyloid immunoassays and visual amyloid positron emission tomographic assessment 

JAMA Neurology 2017 Dec 1;74(12):1492-1501.

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Atrophy of the posterior subiculum is associated with memory impairment, tau- and Aβ pathology in non-demented individuals.

Frontiers in Aging Neuroscience. 2017 Sep 20;9:306.

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In vivo retention of (18)F-AV-1451 in corticobasal syndrome.

Neurology. 2017 Aug 22;89(8):845-853.

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

Brain 2017 Sep 1;140(9):2286-2294.

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

EMBO Mol Med. 2017 Sep;9(9):1212-1223.

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Recommendations for cerebrospinal fluid collection for the analysis by ELISA of neurogranin trunc P75, α-synuclein, and total tau in combination with Aβ(1-42)/Aβ(1-40).

Alzheimers Res Ther. 2017 Jun 6;9(1):40.

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Psychometric testing of a Swedish version of the Apathy Evaluation Scale.

Nord J Psychiatry. 2017 Aug;71(6):477-484.

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Tau oligomers in cerebrospinal fluid in Alzheimer’s disease.

Ann Clin Transl Neurol. 2017 Mar 1;4(4):226-235.

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Increased blood-brain barrier permeability is associated with dementia and diabetes but not amyloid pathology or APOE genotype.

Neurobiol Aging. 2017 Mar;51:104-112.

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Tau Pathology Distribution in Alzheimer’s disease Corresponds Differentially to Cognition-Relevant Functional Brain Networks.

Front Neurosci. 2017 Mar 31;11:167.

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

Acta Neuropathol. 2017 Jan;133(1):149-151.

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

27 October, 2016

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 (T807) tau binding, including models with blood sampling and non-invasive alternatives. METHODS:

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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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