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[A fruit fly (Drosophila melanogaster) as a model organism for studies of brain diseases].

https://arctichealth.org/en/permalink/ahliterature169705
Source
Duodecim. 2006;122(4):443-50
Publication Type
Article
Date
2006
Author
Liisa Myllykangas
Tapio Heino
Author Affiliation
Folkhälsanin perinnöllisyystieteen laitos jaa Neurotieteen tutkimuskeskus, Biomedicum Helsinki, Helsingin yliopisto. liisa.myllykangas@helsinki.fi
Source
Duodecim. 2006;122(4):443-50
Date
2006
Language
Finnish
Publication Type
Article
Keywords
Animals
Brain Diseases - diagnosis - therapy
Disease Models, Animal
Drosophila melanogaster
Finland
Humans
Sensitivity and specificity
PubMed ID
16623099 View in PubMed
Less detail

alpha-Synuclein pathology in the spinal cord autonomic nuclei associates with alpha-synuclein pathology in the brain: a population-based Vantaa 85+ study.

https://arctichealth.org/en/permalink/ahliterature146471
Source
Acta Neuropathol. 2010 Jun;119(6):715-22
Publication Type
Article
Date
Jun-2010
Author
Minna Oinas
Anders Paetau
Liisa Myllykangas
Irma-Leena Notkola
Hannu Kalimo
Tuomo Polvikoski
Author Affiliation
Department of Pathology, Helsinki University Central Hospital,University of Helsinki, P.O. Box 21, Haartmaninkatu 3, 00014 Helsinki, Finland. minna.oinas@helsinki.fi
Source
Acta Neuropathol. 2010 Jun;119(6):715-22
Date
Jun-2010
Language
English
Publication Type
Article
Keywords
Age Factors
Aged, 80 and over
Autonomic Nervous System - metabolism - pathology
Brain - metabolism - pathology
Brain Diseases - metabolism - pathology
Cohort Studies
Female
Finland
Humans
Immunohistochemistry
Male
Neuropil - metabolism - pathology
Sacrococcygeal Region
Severity of Illness Index
Spinal Cord - metabolism - pathology
Spinal Cord Diseases - metabolism - pathology
Thoracic Vertebrae
alpha-Synuclein - metabolism
Abstract
In most subjects with Parkinson's disease and dementia with Lewy bodies, alpha-synuclein (alphaS) immunoreactive pathology is found not only in the brain but also in the autonomic nuclei of the spinal cord. However, neither has the temporal course of alphaS pathology in the spinal cord in relation to the brain progression been established, nor has the extent of alphaS pathology in the spinal cord been analyzed in population-based studies. Using immunohistochemistry, the frequency and distribution of alphaS pathology were assessed semiquantitatively in the brains and spinal cord nuclei of 304 subjects who were aged at least 85 in the population-based Vantaa 85+ study. alphaS pathology was common in the spinal cord; 102 (34%) subjects had classic alphaS pathology in the thoracic and/or sacral autonomic nuclei. Moreover, 134 (44%) subjects showed grain- or dot-like immunoreactivity in neuropil (mini-aggregates) without classic Lewy neurites or Lewy bodies (LBs). The latter type of alphaS accumulation is associated with age, but also the classic alphaS pathology was found more often in the oldest compared to the youngest age group. The severity of alphaS pathology in the spinal cord autonomic nuclei is significantly associated with the extent and severity of alphaS pathology in the brain. Of the subjects, 60% with moderate to severe thoracic alphaS pathology and up to 89% with moderate to severe sacral alphaS pathology had diffuse neocortical type of LB pathology in the brain. alphaS pathology exclusively in the spinal cord was rare. Our study indicates that in general alphaS pathology in the spinal cord autonomic nuclei is associated with similar pathology in the brain.
PubMed ID
20037761 View in PubMed
Less detail

Amyloid precursor protein (APP) A673T mutation in the elderly Finnish population.

https://arctichealth.org/en/permalink/ahliterature119431
Source
Neurobiol Aging. 2013 May;34(5):1518.e1-3
Publication Type
Article
Date
May-2013
Author
Mia Kero
Anders Paetau
Tuomo Polvikoski
Maarit Tanskanen
Raimo Sulkava
Lilja Jansson
Liisa Myllykangas
Pentti J Tienari
Author Affiliation
Department of Pathology, University of Helsinki and HUSLAB, Helsinki, Finland.
Source
Neurobiol Aging. 2013 May;34(5):1518.e1-3
Date
May-2013
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - metabolism
Amyloid beta-Protein Precursor - genetics
Female
Finland - epidemiology
Humans
Male
Mutation - genetics
Neocortex - physiology
Polymorphism, Single Nucleotide - genetics
Abstract
Pathogenic mutations of the APP gene, leading to early-onset Alzheimer's disease (AD) have been known for more than 20 years. Recently, it was discovered that APP mutations might also be protective. A rare variant A673T reportedly protects against AD and age-related cognitive impairment and might functionally inhibit proteolytic cleavage at the ß-secretase site of APP. We sequenced APP exon 16 in a population-based sample of 515 Finnish subjects aged 85 or older. Neuropathologic data were available in 274. We found the A673T variant in 1 subject (0.2%), who lived until age 104.8 years (second highest age-at-death in the cohort). Neuropathologic analysis showed little beta-amyloid pathology (Consortium to Establish a Registry for Alzheimer's Disease score 0). Some vascular amyloid was detected in meningeal arteries suggesting that vascular ß-amyloid accumulation might be less inhibited than the parenchymal. She was demented at the age of 104, most likely because of hippocampal sclerosis. The low amount of parenchymal ß-amyloid pathology at the age of 104.8 years supports the concept that the A673T variant protects the brain against ß-amyloid pathology and AD.
PubMed ID
23102935 View in PubMed
Less detail

APOE and AßPP gene variation in cortical and cerebrovascular amyloid-ß pathology and Alzheimer's disease: a population-based analysis.

https://arctichealth.org/en/permalink/ahliterature133862
Source
J Alzheimers Dis. 2011;26(2):377-85
Publication Type
Article
Date
2011
Author
Terhi Peuralinna
Maarit Tanskanen
Mira Mäkelä
Tuomo Polvikoski
Anders Paetau
Hannu Kalimo
Raimo Sulkava
John Hardy
Shiao-Lin Lai
Sampath Arepalli
Dena Hernandez
Bryan J Traynor
Andrew Singleton
Pentti J Tienari
Liisa Myllykangas
Author Affiliation
University of Helsinki, Research Program of Molecular Neurology, Biomedicum-Helsinki, Helsinki, Finland.
Source
J Alzheimers Dis. 2011;26(2):377-85
Date
2011
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alleles
Alzheimer Disease - genetics - metabolism - pathology
Amyloid beta-Peptides - genetics - metabolism
Amyloid beta-Protein Precursor - genetics - metabolism
Apolipoproteins E - genetics - metabolism
Cerebral Amyloid Angiopathy - genetics - metabolism - pathology
Cerebral Cortex - metabolism - pathology
Female
Finland
Genetic Association Studies
Genetic Variation
Humans
Male
Middle Aged
Phenotype
Promoter Regions, Genetic
Abstract
Cortical and cerebrovascular amyloid-? (A?) deposition is a hallmark of Alzheimer's disease (AD), but also occurs in elderly people not affected by dementia. The apolipoprotein E (APOE) e4 is a major genetic modulator of A? deposition and AD risk. Variants of the amyloid-? protein precursor (A?PP) gene have been reported to contribute to AD and cerebral amyloid angiopathy (CAA). We analyzed the role of APOE and A?PP variants in cortical and cerebrovascular A? deposition, and neuropathologically verified AD (based on modified NIA-RI criteria) in a population-based autopsy sample of Finns aged = 85 years (Vantaa85 + Study; n = 282). Our updated analysis of APOE showed strong associations of the e4 allele with cortical (p = 4.91 ? 10-17) and cerebrovascular (p = 9.87 ? 10-11) A? deposition as well as with NIA-RI AD (p = 1.62 ? 10-8). We also analyzed 60 single nucleotide polymorphisms (SNPs) at the A?PP locus. In single SNP or haplotype analyses there were no statistically significant A?PP locus associations with cortical or cerebrovascular A? deposition or with NIA-RI AD. We sequenced the promoter of the A?PP gene in 40 subjects with very high A? deposition, but none of these subjects had any of the previously reported or novel AD-associated mutations. These results suggest that cortical and cerebrovascular A? depositions are useful quantitative traits for genetic studies, as highlighted by the strong associations with the APOE e4 variant. Promoter mutations or common allelic variation in the A?PP gene do not have a major contribution to cortical or cerebrovascular A? deposition, or very late-onset AD in this Finnish population based study.
Notes
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PubMed ID
21654062 View in PubMed
Less detail

Capillary amyloid-ß protein deposition in a population-based study (Vantaa 85+).

https://arctichealth.org/en/permalink/ahliterature276368
Source
J Alzheimers Dis. 2015;49(1):149-57
Publication Type
Article
Date
2015
Author
Mira Mäkelä
Anders Paetau
Tuomo Polvikoski
Liisa Myllykangas
Maarit Tanskanen
Source
J Alzheimers Dis. 2015;49(1):149-57
Date
2015
Language
English
Publication Type
Article
Keywords
Aged, 80 and over
Alzheimer Disease - pathology
Amyloid beta-Peptides - metabolism
Apolipoprotein E4 - genetics
Autopsy
Capillaries - pathology
Cerebral Amyloid Angiopathy - pathology
Female
Finland
Genotype
Humans
Immunohistochemistry
Logistic Models
Male
Multivariate Analysis
Occipital Lobe - pathology
Prospective Studies
Severity of Illness Index
Abstract
Capillary amyloid-ß (capAß) deposition in the cerebral cortex is the neuropathological feature providing the basis for categorizing cerebral amyloid angiopathy (CAA) into two distinct types, CAA-Type1 with capAß and CAA-Type2 without capAß.
We investigated the neuropathological and clinical characteristics of capAß deposition in a prospective population-based study.
Vantaa 85+ includes 601 individuals aged =85 years, of which 300 were studied clinically and neuropathologically. 278 subjects were analyzed for the apolipoprotein E (APOE) genotype. The diagnosis of capAß was determined using immunohistochemistry against Aß, and of CAA using Congo red confirmed by Aß immunohistochemistry, both analyzed in six brain areas. The severity of capAß was graded semi-quantitatively, and the severity of CAA was based on the percentage of affected vessels. Alzheimer's disease (AD)-type neuropathology (CERAD score and Braak stage) was analyzed using standard methods.
CAA-Type1 was present in 86/300, CAA-Type2 in 135/300, and 79/300 had no CAA. CapAß was most frequent in the occipital lobe (79/86). CAA-Type1 was associated with the severity of CAA (p?
PubMed ID
26444758 View in PubMed
Less detail

Chromosome 9 ALS and FTD locus is probably derived from a single founder.

https://arctichealth.org/en/permalink/ahliterature131202
Source
Neurobiol Aging. 2012 Jan;33(1):209.e3-8
Publication Type
Article
Date
Jan-2012
Author
Kin Mok
Bryan J Traynor
Jennifer Schymick
Pentti J Tienari
Hannu Laaksovirta
Terhi Peuralinna
Liisa Myllykangas
Adriano Chiò
Aleksey Shatunov
Bradley F Boeve
Adam L Boxer
Mariely DeJesus-Hernandez
Ian R Mackenzie
Adrian Waite
Nigel Williams
Huw R Morris
Javier Simón-Sánchez
John C van Swieten
Peter Heutink
Gabriella Restagno
Gabriele Mora
Karen E Morrison
Pamela J Shaw
Pamela Sara Rollinson
Ammar Al-Chalabi
Rosa Rademakers
Stuart Pickering-Brown
Richard W Orrell
Michael A Nalls
John Hardy
Author Affiliation
Reta Lila Weston Research Laboratories, Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK.
Source
Neurobiol Aging. 2012 Jan;33(1):209.e3-8
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Amyotrophic Lateral Sclerosis - genetics
Chromosomes, Human, Pair 9 - genetics
Finland
Frontotemporal Dementia - genetics
Genetic Linkage
Genome-Wide Association Study
Haplotypes
Humans
Polymorphism, Single Nucleotide
Abstract
We and others have recently reported an association between amyotrophic lateral sclerosis (ALS) and single nucleotide polymorphisms on chromosome 9p21 in several populations. Here we show that the associated haplotype is the same in all populations and that several families previously shown to have genetic linkage to this region also share this haplotype. The most parsimonious explanation of these data are that there is a single founder for this form of disease.
Notes
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PubMed ID
21925771 View in PubMed
Less detail

Chromosome 9p21 in amyotrophic lateral sclerosis in Finland: a genome-wide association study.

https://arctichealth.org/en/permalink/ahliterature141194
Source
Lancet Neurol. 2010 Oct;9(10):978-85
Publication Type
Article
Date
Oct-2010
Author
Hannu Laaksovirta
Terhi Peuralinna
Jennifer C Schymick
Sonja W Scholz
Shaoi-Lin Lai
Liisa Myllykangas
Raimo Sulkava
Lilja Jansson
Dena G Hernandez
J Raphael Gibbs
Michael A Nalls
David Heckerman
Pentti J Tienari
Bryan J Traynor
Author Affiliation
Department of Neurology, Helsinki University Central Hospital and Molecular Neurology Programme, Biomedicum, University of Helsinki, Helsinki, Finland.
Source
Lancet Neurol. 2010 Oct;9(10):978-85
Date
Oct-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Amyotrophic Lateral Sclerosis - enzymology - epidemiology - genetics
Chromosomes, Human, Pair 9 - genetics
Cohort Studies
Female
Finland - epidemiology
Genetic Loci - genetics
Genetic Predisposition to Disease - epidemiology - genetics
Genome-Wide Association Study - methods
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Superoxide Dismutase - genetics
Young Adult
Abstract
The genetic cause of amyotrophic lateral sclerosis (ALS) is not well understood. Finland is a well suited location for a genome-wide association study of ALS because the incidence of the disease is one of the highest in the world, and because the genetic homogeneity of the Finnish population enhances the ability to detect risk loci. We aimed to identify genetic risk factors for ALS in the Finnish population.
We did a genome-wide association study of Finnish patients with ALS and control individuals by use of Illumina genome-wide genotyping arrays. DNA was collected from patients who attended an ALS specialty clinic that receives referrals from neurologists throughout Finland. Control samples were from a population-based study of elderly Finnish individuals. Patients known to carry D90A alleles of the SOD1 gene (n=40) were included in the final analysis as positive controls to assess whether our genome-wide association study was able to detect an association signal at this locus.
We obtained samples from 442 patients with ALS and 521 control individuals. After quality control filters were applied, 318?167 single nucleotide polymorphisms (SNPs) from 405 people with ALS and 497 control individuals were available for analysis. We identified two association peaks that exceeded genome-wide significance. One was located on chromosome 21q22 (rs13048019, p=2·58×10(-8)), which corresponds to the autosomal recessive D90A allele of the SOD1 gene. The other was detected in a 232 kb block of linkage disequilibrium (rs3849942, p=9·11×10(-11)) in a region of chromosome 9p that was previously identified in linkage studies of families with ALS. Within this region, we defined a 42-SNP haplotype that was associated with significantly increased risk of ALS (p=7·47×10(-33) when people with familial ALS were compared with controls, odds ratio 21·0, 95% CI 11·2-39·1) and which overlapped with an association locus recently reported for frontotemporal dementia. For the 93 patients with familial ALS, the population attributable risk for the chromosome 9p21 locus was 37·9% (95% CI 27·7-48·1) and that for D90A homozygosity was 25·5% (16·9-34·1).
The chromosome 9p21 locus is a major cause of familial ALS in the Finnish population. Our data suggest the presence of a founder mutation for chromosome 9p21-linked ALS. Furthermore, the overlap with the risk haplotype recently reported for frontotemporal dementia provides further evidence of a shared genetic cause for these two neurodegenerative diseases.
National Institutes of Health and National Institute on Aging, Microsoft Research, ALS Association, Helsinki University Central Hospital, Finnish Academy, Finnish Medical Society Duodecim, and Kuopio University.
Notes
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Comment In: Lancet Neurol. 2010 Oct;9(10):945-720801719
PubMed ID
20801718 View in PubMed
Less detail

Fatal Tick-Borne Encephalitis Virus Infections Caused by Siberian and European Subtypes, Finland, 2015.

https://arctichealth.org/en/permalink/ahliterature298365
Source
Emerg Infect Dis. 2018 05; 24(5):946-948
Publication Type
Case Reports
Letter
Research Support, Non-U.S. Gov't
Date
05-2018
Author
Suvi Kuivanen
Teemu Smura
Kirsi Rantanen
Leena Kämppi
Jonas Kantonen
Mia Kero
Anu Jääskeläinen
Anne J Jääskeläinen
Jussi Sane
Liisa Myllykangas
Anders Paetau
Olli Vapalahti
Source
Emerg Infect Dis. 2018 05; 24(5):946-948
Date
05-2018
Language
English
Publication Type
Case Reports
Letter
Research Support, Non-U.S. Gov't
Keywords
Adult
Aged
Animals
Encephalitis Viruses, Tick-Borne - genetics
Encephalitis, Tick-Borne - epidemiology - virology
Fatal Outcome
Female
Finland - epidemiology
Humans
Male
RNA, Viral - genetics - isolation & purification
Ticks - virology
Abstract
In most locations except for Russia, tick-borne encephalitis is mainly caused by the European virus subtype. In 2015, fatal infections caused by European and Siberian tick-borne encephalitis virus subtypes in the same Ixodes ricinus tick focus in Finland raised concern over further spread of the Siberian subtype among widespread tick species.
PubMed ID
29664395 View in PubMed
Less detail

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.

https://arctichealth.org/en/permalink/ahliterature131029
Source
Neuron. 2011 Oct 20;72(2):257-68
Publication Type
Article
Date
Oct-20-2011
Author
Alan E Renton
Elisa Majounie
Adrian Waite
Javier Simón-Sánchez
Sara Rollinson
J Raphael Gibbs
Jennifer C Schymick
Hannu Laaksovirta
John C van Swieten
Liisa Myllykangas
Hannu Kalimo
Anders Paetau
Yevgeniya Abramzon
Anne M Remes
Alice Kaganovich
Sonja W Scholz
Jamie Duckworth
Jinhui Ding
Daniel W Harmer
Dena G Hernandez
Janel O Johnson
Kin Mok
Mina Ryten
Danyah Trabzuni
Rita J Guerreiro
Richard W Orrell
James Neal
Alex Murray
Justin Pearson
Iris E Jansen
David Sondervan
Harro Seelaar
Derek Blake
Kate Young
Nicola Halliwell
Janis Bennion Callister
Greg Toulson
Anna Richardson
Alex Gerhard
Julie Snowden
David Mann
David Neary
Michael A Nalls
Terhi Peuralinna
Lilja Jansson
Veli-Matti Isoviita
Anna-Lotta Kaivorinne
Maarit Hölttä-Vuori
Elina Ikonen
Raimo Sulkava
Michael Benatar
Joanne Wuu
Adriano Chiò
Gabriella Restagno
Giuseppe Borghero
Mario Sabatelli
David Heckerman
Ekaterina Rogaeva
Lorne Zinman
Jeffrey D Rothstein
Michael Sendtner
Carsten Drepper
Evan E Eichler
Can Alkan
Ziedulla Abdullaev
Svetlana D Pack
Amalia Dutra
Evgenia Pak
John Hardy
Andrew Singleton
Nigel M Williams
Peter Heutink
Stuart Pickering-Brown
Huw R Morris
Pentti J Tienari
Bryan J Traynor
Author Affiliation
Neuromuscular Diseases Research Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
Source
Neuron. 2011 Oct 20;72(2):257-68
Date
Oct-20-2011
Language
English
Publication Type
Article
Keywords
Alleles
Amyotrophic Lateral Sclerosis - genetics
Chromosomes, Human, Pair 9
Female
Finland
Frontotemporal Dementia - genetics
Genetic Predisposition to Disease
Genotype
Haplotypes
Humans
Male
Microsatellite Repeats
Pedigree
Polymorphism, Single Nucleotide
Abstract
The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases. We have previously shown that a founder haplotype, covering the MOBKL2b, IFNK, and C9ORF72 genes, is present in the majority of cases linked to this region. Here we show that there is a large hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72 on the affected haplotype. This repeat expansion segregates perfectly with disease in the Finnish population, underlying 46.0% of familial ALS and 21.1% of sporadic ALS in that population. Taken together with the D90A SOD1 mutation, 87% of familial ALS in Finland is now explained by a simple monogenic cause. The repeat expansion is also present in one-third of familial ALS cases of outbred European descent, making it the most common genetic cause of these fatal neurodegenerative diseases identified to date.
Notes
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PubMed ID
21944779 View in PubMed
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Melatonin receptor type 1A gene linked to Alzheimer's disease in old age.

https://arctichealth.org/en/permalink/ahliterature299161
Source
Sleep. 2018 07 01; 41(7):
Publication Type
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Date
07-01-2018
Author
Sonja Sulkava
Pranuthi Muggalla
Raimo Sulkava
Hanna M Ollila
Terhi Peuralinna
Liisa Myllykangas
Karri Kaivola
David J Stone
Bryan J Traynor
Alan E Renton
Alberto M Rivera
Seppo Helisalmi
Hilkka Soininen
Tuomo Polvikoski
Mikko Hiltunen
Pentti J Tienari
Henri J Huttunen
Tiina Paunio
Author Affiliation
Department of Health, Genomics and Biomarkers Unit, National Institute for Health and Welfare, Helsinki, Finland.
Source
Sleep. 2018 07 01; 41(7):
Date
07-01-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Keywords
Aged, 80 and over
Alzheimer Disease - genetics - pathology
Amyloid beta-Peptides - metabolism
Amyloid beta-Protein Precursor - metabolism
Brain - metabolism - pathology
Case-Control Studies
Circadian Rhythm
Cohort Studies
Female
Finland
Genetic Predisposition to Disease
Humans
In Vitro Techniques
Male
Melatonin - metabolism
Neurofibrillary Tangles - genetics - pathology
Neurons - metabolism
Plaque, Amyloid - genetics - pathology
Receptor, Melatonin, MT1 - genetics - metabolism
Receptors, Melatonin
Abstract
Disruption of the circadian rhythms is a frequent preclinical and clinical manifestation of Alzheimer's disease. Furthermore, it has been suggested that shift work is a risk factor for Alzheimer's disease. Previously, we have reported association of intolerance to shift work (job-related exhaustion in shift workers) with a variant rs12506228A, which is situated close to melatonin receptor type 1A gene (MTNR1A) and linked to MTNR1A brain expression levels. Here, we studied association of that variant with clinical and neuropathological Alzheimer's disease in a Finnish whole-population cohort Vantaa 85+ (n = 512, participants over 85 years) and two follow-up cohorts. Rs12506228A was associated with clinical Alzheimer's disease (p = 0.000073). Analysis of post-mortem brain tissues showed association with higher amount of neurofibrillary tangles (p = 0.0039) and amyloid beta plaques (p = 0.0041). We then followed up the associations in two independent replication samples. Replication for the association with clinical Alzheimer's disease was detected in Kuopio 75+ (p = 0.012, n = 574), but not in the younger case-control sample (n = 651 + 669). While melatonin has been established in regulation of circadian rhythms, an independent role has been also shown for neuroprotection and specifically for anti-amyloidogenic effects. Indeed, in vitro, RNAi mediated silencing of MTNR1A increased the amyloidogenic processing of amyloid precursor protein (APP) in neurons, whereas overexpression decreased it. Our findings suggest variation close to MTNR1A as a shared genetic risk factor for intolerance to shift work and Alzheimer's disease in old age. The genetic associations are likely to be mediated by differences in MTNR1A expression, which, in turn, modulate APP metabolism.
PubMed ID
29982836 View in PubMed
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