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

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

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

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

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)

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

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

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

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

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

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

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

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

Sci Adv. 2020 Nov 27;6(48)

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

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

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

Prog Neurobiol. 2020 Aug 31:101904.

Neuroimage Clin. 2020;28:102386.

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Neuroimage Clin. 2020 Jun 10;27:102310.

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

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

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

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

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

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

JAMA Neurol. 2020 May 11:e200989.

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

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

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

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

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

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

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

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

Neurobiol Dis. 2020 Feb;134:104645.

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

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

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

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

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

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

Elife. 2019 Dec 9;8:e50830.

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

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

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

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

Commun Biol. 2019 Oct 8;2:365.

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

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

PLoS One. 2019 Sep 4;14(9):e0222002.

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

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

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

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

JAMA Neurol. 2019 Jul 17;76(11)

Parkinsonism Relat Disord. 2019 Sep 6.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

JAMA Neurol. 2019 Mar; 76(3): 310–31

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Front Neurosci. 2017 Mar 31;11:167.

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

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

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

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:

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

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

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

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

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.

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

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

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

J Neurochem. 2016 Nov;139(4):651-658

EMBO Mol Med. 2016 Oct 4;8(10):1184-1196

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,

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

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

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

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

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

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

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

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.

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,

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

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

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

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

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

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

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

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,

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

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

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

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

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

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

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

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

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

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