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A 9-year prospective population-based study on the association between the APOE*E4 allele and late-life depression in Sweden.

https://arctichealth.org/en/permalink/ahliterature274872
Source
Biol Psychiatry. 2015 Nov 15;78(10):730-6
Publication Type
Article
Date
Nov-15-2015
Author
Ingmar Skoog
Margda Waern
Paul Duberstein
Kaj Blennow
Henrik Zetterberg
Anne Börjesson-Hanson
Svante Östling
Xinxin Guo
Jürgen Kern
Deborah Gustafson
Pia Gudmundsson
Thomas Marlow
Silke Kern
Source
Biol Psychiatry. 2015 Nov 15;78(10):730-6
Date
Nov-15-2015
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Apolipoprotein E4 - genetics
Depressive Disorder - epidemiology - genetics
Depressive Disorder, Major - epidemiology - genetics
Female
Follow-Up Studies
Humans
Late Onset Disorders - epidemiology - genetics
Male
Prospective Studies
Sweden - epidemiology
Abstract
It is well established that there is an association between the apolipoprotein E (APOE) e4 allele (APOE*E4) and Alzheimer's disease. It is less clear whether there is also an association with geriatric depression. We examined the relationship between APOE*E4 and 5-year incidence of depression in a Swedish population-based sample of older adults without dementia and excluding older adults who developed dementia within 4 years after the diagnosis of depression.
In 2000-2001, 839 women and men (age range, 70-92 years; mean age, 73.8 years) free from dementia and depression underwent neuropsychiatric and neuropsychological examinations and genotyping of the APOE*E4 allele. Follow-up evaluations were conducted in 2005 and 2009.The association between APOE*E4 allele and 5-year incidence of depression was examined, while avoiding possible confounding effects of clinical or preclinical dementia by excluding participants who had dementia at study entry, subsequently developed dementia during the 9-year follow-up period, or had a decline in Mini-Mental State Examination score of =5 points.
Among subjects without depression at study entry and without dementia or significant cognitive decline during the subsequent 9 years, APOE*E4 was prospectively associated with more severe depressive symptoms (b = 1.56, p = .007), incident minor depression (odds ratio = 1.99 [confidence interval = 1.11-3.55], p = .020), and any depression (odds ratio = 1.75 [confidence interval = 1.01-3.03], p = .048).
The presence of the APOE*E4 allele predicted future depression in this Swedish population study, even after excluding depressed individuals who later developed dementia, suggesting that the APOE*E4 allele could potentially identify people at high risk for clinically significant depression.
Notes
Comment In: Biol Psychiatry. 2015 Nov 15;78(10):670-126497282
PubMed ID
25708227 View in PubMed
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A 10-Year Follow-Up of Adiposity and Dementia in Swedish Adults Aged 70 Years and Older.

https://arctichealth.org/en/permalink/ahliterature300956
Source
J Alzheimers Dis. 2018; 63(4):1325-1335
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
2018
Author
Ilse A C Arnoldussen
Valter Sundh
Kristoffer Bäckman
Silke Kern
Svante Östling
Kaj Blennow
Henrik Zetterberg
Ingmar Skoog
Amanda J Kiliaan
Deborah R Gustafson
Author Affiliation
Department of Anatomy, Donders Institute for Brain, Cognition and Behaviour, Radboud university medical center, Nijmegen, The Netherlands.
Source
J Alzheimers Dis. 2018; 63(4):1325-1335
Date
2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adiponectin - blood
Adiposity
Aged
Aged, 80 and over
Anthropometry
Body mass index
Dementia - blood - epidemiology - pathology
Fasting
Female
Humans
Independent living
Leptin - blood
Longitudinal Studies
Male
Psychiatric Status Rating Scales
Sex Factors
Sweden - epidemiology
Waist-Hip Ratio
Abstract
Adiposity measured in mid- or late-life and estimated using anthropometric measures such as body mass index (BMI) and waist-to-hip ratio (WHR), or metabolic markers such as blood leptin and adiponectin levels, is associated with late-onset dementia risk. However, during later life, this association may reverse and aging- and dementia-related processes may differentially affect adiposity measures.
We explored associations of concurrent BMI, WHR, and blood leptin and high molecular weight adiponectin levels with dementia occurrence.
924 Swedish community-dwelling elderly without dementia, aged 70 years and older, systematically-sampled by birth day and birth year population-based in the Gothenburg city region of Sweden. The Gothenburg Birth Cohort Studies are designed for evaluating risk and protective factors for dementia. All dementias diagnosed after age 70 for 10 years were identified. Multivariable logistic regression models were used to predict dementia occurrence between 2000-2005, 2005-2010, and 2000-2010 after excluding prevalent baseline (year 2000) dementias. Baseline levels of BMI, WHR, leptin, and adiponectin were used.
Within 5 years of baseline, low BMI (
PubMed ID
29758945 View in PubMed
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The Alzheimer's Association external quality control program for cerebrospinal fluid biomarkers.

https://arctichealth.org/en/permalink/ahliterature132754
Source
Alzheimers Dement. 2011 Jul;7(4):386-395.e6
Publication Type
Article
Date
Jul-2011
Author
Niklas Mattsson
Ulf Andreasson
Staffan Persson
Hiroyuki Arai
Sat Dev Batish
Sergio Bernardini
Luisella Bocchio-Chiavetto
Marinus A Blankenstein
Maria C Carrillo
Sonia Chalbot
Els Coart
Davide Chiasserini
Neal Cutler
Gunilla Dahlfors
Stefan Duller
Anne M Fagan
Orestes Forlenza
Giovanni B Frisoni
Douglas Galasko
Daniela Galimberti
Harald Hampel
Aase Handberg
Michael T Heneka
Adrianna Z Herskovits
Sanna-Kaisa Herukka
David M Holtzman
Christian Humpel
Bradley T Hyman
Khalid Iqbal
Mathias Jucker
Stephan A Kaeser
Elmar Kaiser
Elisabeth Kapaki
Daniel Kidd
Peter Klivenyi
Cindy S Knudsen
Markus P Kummer
James Lui
Albert Lladó
Piotr Lewczuk
Qiao-Xin Li
Ralph Martins
Colin Masters
John McAuliffe
Marc Mercken
Abhay Moghekar
José Luis Molinuevo
Thomas J Montine
William Nowatzke
Richard O'Brien
Markus Otto
George P Paraskevas
Lucilla Parnetti
Ronald C Petersen
David Prvulovic
Herman P M de Reus
Robert A Rissman
Elio Scarpini
Alessandro Stefani
Hilkka Soininen
Johannes Schröder
Leslie M Shaw
Anders Skinningsrud
Brith Skrogstad
Annette Spreer
Leda Talib
Charlotte Teunissen
John Q Trojanowski
Hayrettin Tumani
Robert M Umek
Bianca Van Broeck
Hugo Vanderstichele
Laszlo Vecsei
Marcel M Verbeek
Manfred Windisch
Jing Zhang
Henrik Zetterberg
Kaj Blennow
Author Affiliation
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden. niklas.mattsson@neuro.gu.se
Source
Alzheimers Dement. 2011 Jul;7(4):386-395.e6
Date
Jul-2011
Language
English
Publication Type
Article
Keywords
Alzheimer Disease - cerebrospinal fluid - diagnosis
Amyloid beta-Peptides - cerebrospinal fluid
Biological Assay - methods
Biological Markers - cerebrospinal fluid
Enzyme-Linked Immunosorbent Assay
Humans
Peptide Fragments - cerebrospinal fluid
Phosphorylation
Quality Control
Reproducibility of Results
Sweden
Time Factors
tau Proteins - cerebrospinal fluid
Abstract
The cerebrospinal fluid (CSF) biomarkers amyloid ß (Aß)-42, total-tau (T-tau), and phosphorylated-tau (P-tau) demonstrate good diagnostic accuracy for Alzheimer's disease (AD). However, there are large variations in biomarker measurements between studies, and between and within laboratories. The Alzheimer's Association has initiated a global quality control program to estimate and monitor variability of measurements, quantify batch-to-batch assay variations, and identify sources of variability. In this article, we present the results from the first two rounds of the program.
The program is open for laboratories using commercially available kits for Aß, T-tau, or P-tau. CSF samples (aliquots of pooled CSF) are sent for analysis several times a year from the Clinical Neurochemistry Laboratory at the Mölndal campus of the University of Gothenburg, Sweden. Each round consists of three quality control samples.
Forty laboratories participated. Twenty-six used INNOTEST enzyme-linked immunosorbent assay kits, 14 used Luminex xMAP with the INNO-BIA AlzBio3 kit (both measure Aß-(1-42), P-tau(181P), and T-tau), and 5 used Meso Scale Discovery with the Aß triplex (AßN-42, AßN-40, and AßN-38) or T-tau kits. The total coefficients of variation between the laboratories were 13% to 36%. Five laboratories analyzed the samples six times on different occasions. Within-laboratory precisions differed considerably between biomarkers within individual laboratories.
Measurements of CSF AD biomarkers show large between-laboratory variability, likely caused by factors related to analytical procedures and the analytical kits. Standardization of laboratory procedures and efforts by kit vendors to increase kit performance might lower variability, and will likely increase the usefulness of CSF AD biomarkers.
Notes
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Erratum In: Alzheimers Dement. 2011 Sep;7(5):556
PubMed ID
21784349 View in PubMed
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Association of NFE2L2 and KEAP1 haplotypes with amyotrophic lateral sclerosis.

https://arctichealth.org/en/permalink/ahliterature257631
Source
Amyotroph Lateral Scler Frontotemporal Degener. 2014 Mar;15(1-2):130-7
Publication Type
Article
Date
Mar-2014
Author
Petra Bergström
Malin von Otter
Staffan Nilsson
Ann-Charloth Nilsson
Michael Nilsson
Peter M Andersen
Ola Hammarsten
Henrik Zetterberg
Author Affiliation
Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy at the University of Gothenburg , Gothenburg , Sweden.
Source
Amyotroph Lateral Scler Frontotemporal Degener. 2014 Mar;15(1-2):130-7
Date
Mar-2014
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Aged
Aged, 80 and over
Amyotrophic Lateral Sclerosis - genetics
Bulbar Palsy, Progressive - genetics
Female
Gene Frequency
Genetic Association Studies
Genetic Predisposition to Disease - genetics
Haplotypes
Humans
Intracellular Signaling Peptides and Proteins - genetics
Male
Middle Aged
Muscular Atrophy, Spinal - genetics
NF-E2-Related Factor 2 - genetics
Polymorphism, Single Nucleotide - genetics
Promoter Regions, Genetic - genetics
Sweden
Abstract
Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron syndrome influenced by oxidative stress. The transcription factor Nrf2 and its repressor Keap1 constitute an important defence system in cellular protection against oxidative stress. Here we hypothesize that common genetic variations in the genes NFE2L2 and KEAP1, encoding Nrf2 and Keap1, may influence the risk and phenotype of ALS. Five hundred and twenty-two Swedish patients with sporadic ALS (SALS) and 564 Swedish control subjects were studied. Eight tag SNPs in NFE2L2 and three tag SNPs in KEAP1 were genotyped by allelic discrimination and three functional NFE2L2 promoter SNPs were genotyped by sequencing. One NFE2L2 haplotype (GGGAC) was associated with decreased risk of SALS (OR = 0.62 per allele, p = 0.003) and one haplotype in KEAP1 (CGG) was associated with later SALS onset (+3.4 years per allele, p = 0.015). When stratified by subgroup, one haplotype in NFE2L2, GAGCAGA including three functional promoter SNPs associated with high Nrf2 protein expression, was associated with 4.0 years later disease onset per allele in subgroup ALS (p = 0.008). In conclusion, these results suggest that variations in NFE2L2 and KEAP1, encoding two central proteins in cellular oxidative stress defence, may influence SALS pathogenesis.
PubMed ID
24102512 View in PubMed
Less detail

Benchmarking biomarker-based criteria for Alzheimer's disease: Data from the Swedish Dementia Registry, SveDem.

https://arctichealth.org/en/permalink/ahliterature275965
Source
Alzheimers Dement. 2015 Dec;11(12):1470-9
Publication Type
Article
Date
Dec-2015
Author
Christoffer Rosén
Bahman Farahmand
Tobias Skillbäck
Katarina Nägga
Niklas Mattsson
Lena Kilander
Dorota Religa
Anders Wimo
Kaj Blennow
Bengt Winblad
Henrik Zetterberg
Maria Eriksdotter
Source
Alzheimers Dement. 2015 Dec;11(12):1470-9
Date
Dec-2015
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alzheimer Disease - cerebrospinal fluid
Amyloid beta-Peptides - cerebrospinal fluid
Benchmarking - methods
Biomarkers - cerebrospinal fluid
Female
Humans
Male
Middle Aged
Peptide Fragments - cerebrospinal fluid
Phosphorylation
Registries
Sex Factors
Sweden
tau Proteins - cerebrospinal fluid
Abstract
New research guidelines for the diagnosis of Alzheimer's disease (AD) include biomarker evidence of amyloid-ß (Aß) and tau pathology. The aim of this study was to investigate what proportion of AD patients diagnosed in clinical routine in Sweden that had an AD-indicative cerebrospinal fluid (CSF) biomarker profile.
By cross-referencing a laboratory database with the Swedish Dementia Registry (SveDem), 2357 patients with data on CSF Aß and tau biomarkers and a clinical diagnosis of AD with dementia were acquired.
Altogether, 77.2% had pathologic Aß42 and total tau or phosphorylated tau in CSF. These results were stable across age groups. Female sex and low mini-mental state examination score increased the likelihood of pathologic biomarkers.
About a quarter of clinically diagnosed AD patients did not have an AD-indicative CSF biomarker profile. This discrepancy may partly reflect incorrect (false positive) clinical diagnosis or a lack in sensitivity of the biomarker assays.
PubMed ID
26079415 View in PubMed
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Beneficial effects of increased lysozyme levels in Alzheimer's disease modelled in Drosophila melanogaster.

https://arctichealth.org/en/permalink/ahliterature275664
Source
FEBS J. 2016 Aug 26;
Publication Type
Article
Date
Aug-26-2016
Author
Linnea Sandin
Liza Bergkvist
Sangeeta Nath
Claudia Kielkopf
Camilla Janefjord
Linda Helmfors
Henrik Zetterberg
Kaj Blennow
Hongyun Li
Camilla Nilsberth
Brett Garner
Ann-Christin Brorsson
Katarina Kågedal
Source
FEBS J. 2016 Aug 26;
Date
Aug-26-2016
Language
English
Publication Type
Article
Abstract
Genetic polymorphisms of immune genes that associate with higher risk to develop Alzheimer's disease (AD) have led to an increased research interest on the involvement of the immune system in AD pathogenesis. A link between amyloid pathology and immune gene expression was suggested in a genome-wide gene expression study of transgenic amyloid mouse models. In this study, the gene expression of lysozyme, a major player in the innate immune system, was found to be increased in a comparable pattern as the amyloid pathology developed in transgenic mouse models of AD. A similar pattern was seen at protein levels of lysozyme in human AD brain and CSF, but this lysozyme pattern was not seen in a tau transgenic mouse model. Lysozyme was demonstrated to be beneficial for different Drosophila melanogaster models of AD. In flies that expressed Aß1-42 or AßPP together with BACE1 in the eyes, the rough eye phenotype indicative of toxicity was completely rescued by coexpression of lysozyme. In Drosophila flies bearing the Aß1-42 variant with the Arctic gene mutation, lysozyme increased the fly survival and decreased locomotor dysfunction dose dependently. An interaction between lysozyme and Aß1-42 in the Drosophila eye was discovered. We propose that the increased levels of lysozyme, seen in mouse models of AD and in human AD cases, were triggered by Aß1-42 and caused a beneficial effect by binding of lysozyme to toxic species of Aß1-42 , which prevented these from exerting their toxic effects. These results emphasize the possibility of lysozyme as biomarker and therapeutic target for AD.
PubMed ID
27562772 View in PubMed
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Blood biomarkers for brain injury in concussed professional ice hockey players.

https://arctichealth.org/en/permalink/ahliterature104730
Source
JAMA Neurol. 2014 Jun;71(6):684-92
Publication Type
Article
Date
Jun-2014
Author
Pashtun Shahim
Yelverton Tegner
David H Wilson
Jeffrey Randall
Tobias Skillbäck
David Pazooki
Birgitta Kallberg
Kaj Blennow
Henrik Zetterberg
Source
JAMA Neurol. 2014 Jun;71(6):684-92
Date
Jun-2014
Language
English
Publication Type
Article
Keywords
Adult
Athletes
Biological Markers - blood
Brain Concussion - diagnosis
Cohort Studies
Decision Making
Hockey - injuries - physiology
Humans
Male
Neuropsychological Tests
Prospective Studies
Sweden
Young Adult
Abstract
Lack of objective biomarkers for brain damage hampers acute diagnosis and clinical decision making about return to play after sports-related concussion.
To determine whether sports-related concussion is associated with elevated levels of blood biochemical markers of injury to the central nervous system and to assess whether plasma levels of these biomarkers predict return to play in professional ice hockey players with sports-related concussion.
Multicenter prospective cohort study involving all 12 teams of the top professional ice hockey league in Sweden, the Swedish Hockey League. Two hundred eighty-eight professional ice hockey players from 12 teams contesting during the 2012-2013 season consented to participate. All players underwent clinical preseason baseline testing regarding concussion assessment measures. Forty-seven players from 2 of the 12 ice hockey teams underwent blood sampling prior to the start of the season. Thirty-five players had a concussion from September 13, 2012, to January 31, 2013; of these players, 28 underwent repeated blood sampling at 1, 12, 36, and 144 hours and when the players returned to play.
Total tau, S-100 calcium-binding protein B, and neuron-specific enolase concentrations in plasma and serum were measured.
Concussed players had increased levels of the axonal injury biomarker total tau(median, 10.0 pg/mL; range, 2.0-102 pg/mL) compared with preseason values (median, 4.5pg/mL; range, 0.06-22.7 pg/mL) (P
Notes
Comment In: JAMA Neurol. 2014 Jul 1;71(7):925-625023555
Comment In: JAMA Neurol. 2014 Jun;71(6):677-824627000
Comment In: JAMA Neurol. 2014 Jul 1;71(7):926-725023557
PubMed ID
24627036 View in PubMed
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Calcium supplementation and risk of dementia in women with cerebrovascular disease.

https://arctichealth.org/en/permalink/ahliterature282470
Source
Neurology. 2016 Oct 18;87(16):1674-1680
Publication Type
Article
Date
Oct-18-2016
Author
Jürgen Kern
Silke Kern
Kaj Blennow
Henrik Zetterberg
Margda Waern
Xinxin Guo
Anne Börjesson-Hanson
Ingmar Skoog
Svante Östling
Source
Neurology. 2016 Oct 18;87(16):1674-1680
Date
Oct-18-2016
Language
English
Publication Type
Article
Keywords
Aged
Apolipoprotein E4 - genetics
Brain - diagnostic imaging
Calcium, Dietary - administration & dosage
Cortisone - administration & dosage
Dementia - complications - diet therapy - epidemiology - genetics
Dietary Supplements
Estrogens - administration & dosage
Female
Follow-Up Studies
Hormone Replacement Therapy
Humans
Longitudinal Studies
Osteoporotic Fractures - complications - diet therapy - epidemiology - genetics
Prospective Studies
Risk
Stroke - complications - diet therapy - epidemiology - genetics
Sweden
Treatment Failure
Vitamin D - administration & dosage
Abstract
To determine whether calcium supplementation is associated with the development of dementia in women after a 5-year follow-up.
This was a longitudinal population-based study. The sample was derived from the Prospective Population Study of Women and H70 Birth Cohort Study in Gothenburg, Sweden, and included 700 dementia-free women aged 70-92 years. At baseline in 2000-2001, and at follow-up in 2005-2006, the women underwent comprehensive neuropsychiatric and somatic examinations. A CT scan was performed in 447 participants at baseline. Information on the use and dosage of calcium supplements was collected. Dementia was diagnosed according to DSM-III-R criteria.
Women treated with calcium supplements (n = 98) were at a higher risk of developing dementia (odds ratio [OR] 2.10, 95% confidence interval [CI] 1.01-4.37, p = 0.046) and the subtype stroke-related dementia (vascular dementia and mixed dementia) (OR 4.40, 95% CI 1.54-12.61, p = 0.006) than women not given supplementation (n = 602). In stratified analyses, calcium supplementation was associated with the development of dementia in groups with a history of stroke (OR 6.77, 95% CI 1.36-33.75, p = 0.020) or presence of white matter lesions (OR 2.99, 95% CI 1.28-6.96, p = 0.011), but not in groups without these conditions.
Calcium supplementation may increase the risk of developing dementia in elderly women with cerebrovascular disease. Because our sample was relatively small and the study was observational, these findings need to be confirmed.
Notes
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PubMed ID
27534711 View in PubMed
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Cerebrospinal fluid analyses for the diagnosis of subarachnoid haemorrhage and experience from a Swedish study. What method is preferable when diagnosing a subarachnoid haemorrhage?

https://arctichealth.org/en/permalink/ahliterature113419
Source
Clin Chem Lab Med. 2013 Nov;51(11):2073-86
Publication Type
Article
Date
Nov-2013
Author
Karin Nagy
Ina Skagervik
Hayrettin Tumani
Axel Petzold
Manfred Wick
Hans-Jürgen Kühn
Manfred Uhr
Axel Regeniter
Johannes Brettschneider
Markus Otto
Jörg Kraus
Florian Deisenhammer
Ronald Lautner
Kaj Blennow
Leslie Shaw
Henrik Zetterberg
Niklas Mattsson
Source
Clin Chem Lab Med. 2013 Nov;51(11):2073-86
Date
Nov-2013
Language
English
Publication Type
Article
Keywords
Clinical Chemistry Tests - methods
Erythrocyte Count
Humans
Spectrophotometry
Subarachnoid Hemorrhage - blood - cerebrospinal fluid - diagnosis
Sweden
Abstract
Subarachnoid haemorrhage (SAH) has a high mortality and morbidity rate. Early SAH diagnosis allows the early treatment of a ruptured cerebral aneurysm, which improves the prognosis. Diagnostic cerebrospinal fluid (CSF) analyses may be performed after a negative computed tomography scan, but the precise analytical methods to be used have been debated. Here, we summarize the scientific evidence for different CSF methods for SAH diagnosis and describe their implementation in different countries. The principle literature search was conducted using PubMed and Scopus with the search items "cerebrospinal fluid", "subarachnoid haemorrhage", and "diagnosis". CSF analyses for SAH include visual examination, red blood cell counts, spectrophotometry for oxyhaemoglobin or bilirubin determination, CSF cytology, and ferritin measurement. The methods vary in availability and performance. There is a consensus that spectrophotometry has the highest diagnostic performance, but both oxyhaemoglobin and bilirubin determinations are susceptible to important confounding factors. Visual inspection of CSF for xanthochromia is still frequently used for diagnosis of SAH, but it is advised against because spectrophotometry has a superior diagnostic accuracy. A positive finding of CSF bilirubin is a strong indicator of an intracranial bleeding, whereas a positive finding of CSF oxyhaemoglobin may indicate an intracranial bleeding or a traumatic tap. Where spectrophotometry is not available, the combination of CSF cytology for erythrophages or siderophages and ferritin is a promising alternative.
PubMed ID
23729569 View in PubMed
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Cerebrospinal fluid biomarker and brain biopsy findings in idiopathic normal pressure hydrocephalus.

https://arctichealth.org/en/permalink/ahliterature259679
Source
PLoS One. 2014;9(3):e91974
Publication Type
Article
Date
2014
Author
Okko T Pyykkö
Miikka Lumela
Jaana Rummukainen
Ossi Nerg
Toni T Seppälä
Sanna-Kaisa Herukka
Anne M Koivisto
Irina Alafuzoff
Lakshman Puli
Sakari Savolainen
Hilkka Soininen
Juha E Jääskeläinen
Mikko Hiltunen
Henrik Zetterberg
Ville Leinonen
Source
PLoS One. 2014;9(3):e91974
Date
2014
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alzheimer Disease
Amyloid beta-Peptides - cerebrospinal fluid - metabolism
Amyloid beta-Protein Precursor - cerebrospinal fluid - metabolism
Apolipoprotein E4 - cerebrospinal fluid - genetics
Biological Markers - cerebrospinal fluid
Biopsy
Brain - metabolism - pathology
Cytokines - cerebrospinal fluid - metabolism
Female
Finland
Humans
Hydrocephalus, Normal Pressure - cerebrospinal fluid - diagnosis - etiology - pathology
Inflammation Mediators - cerebrospinal fluid - metabolism
Male
Middle Aged
Registries
Abstract
The significance of amyloid precursor protein (APP) and neuroinflammation in idiopathic normal pressure hydrocephalus (iNPH) and Alzheimer's disease (AD) is unknown.
To investigate the role of soluble APP (sAPP) and amyloid beta (Aß) isoforms, proinflammatory cytokines, and biomarkers of neuronal damage in the cerebrospinal fluid (CSF) in relation to brain biopsy Aß and hyperphosphorylated tau (HPt) findings.
The study population comprised 102 patients with possible NPH with cortical brain biopsies, ventricular and lumbar CSF samples, and DNA available. The final clinical diagnoses were: 53 iNPH (91% shunt-responders), 26 AD (10 mixed iNPH+AD), and 23 others. Biopsy samples were immunostained against Aß and HPt. CSF levels of AD-related biomarkers (Aß42, p-tau, total tau), non-AD-related Aß isoforms (Aß38, Aß40), sAPP isoforms (sAPPa, sAPPß), proinflammatory cytokines (several interleukins (IL), interferon-gamma, monocyte chemoattractant protein-1, tumor necrosis factor-alpha) and biomarkers of neuronal damage (neurofilament light and myelin basic protein) were measured. All patients were genotyped for APOE.
Lumbar CSF levels of sAPPa were lower (p
Notes
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PubMed ID
24638077 View in PubMed
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