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A 24-year follow-up of body mass index and cerebral atrophy.

https://arctichealth.org/en/permalink/ahliterature9325
Source
Neurology. 2004 Nov 23;63(10):1876-81
Publication Type
Article
Date
Nov-23-2004
Author
D. Gustafson
L. Lissner
C. Bengtsson
C. Björkelund
I. Skoog
Author Affiliation
Department of Family and Community Medicine, Medical College of Wisconsin, Milwaukee, WI, USA. deb.gustafson@neuro.gu.se
Source
Neurology. 2004 Nov 23;63(10):1876-81
Date
Nov-23-2004
Language
English
Publication Type
Article
Keywords
Adult
Alcohol drinking - epidemiology
Atrophy
Body mass index
Cardiovascular Diseases - epidemiology
Cerebral Cortex - pathology - radiography
Comorbidity
Dementia - epidemiology
Diabetes Mellitus - epidemiology
Educational Status
Female
Follow-Up Studies
Health Surveys
Hormone Replacement Therapy
Humans
Hyperlipidemia - epidemiology
Middle Aged
Obesity - epidemiology - pathology
Research Support, Non-U.S. Gov't
Risk factors
Smoking - epidemiology
Sweden - epidemiology
Tomography, X-Ray Computed
Waist-Hip Ratio
Abstract
OBJECTIVE: To investigate the longitudinal relationship between body mass index (BMI), a major vascular risk factor, and cerebral atrophy, a marker of neurodegeneration, in a population-based sample of middle-aged women. METHODS: A representative sample of 290 women born in 1908, 1914, 1918, and 1922 was examined in 1968 to 1969, 1974 to 1975, 1980 to 1981, and 1992 to 1993 as part of the Population Study of Women in Göteborg, Sweden. At each examination, women completed a survey on a variety of health and lifestyle factors and underwent anthropometric, clinical, and neuropsychiatric assessments and blood collection. Atrophy of the temporal, frontal, occipital, and parietal lobes was measured on CT in 1992 when participants were age 70 to 84. Univariate and multivariate regression analyses were used to assess the relationship between BMI and brain measures. RESULTS: Women with atrophy of the temporal lobe were, on average, 1.1 to 1.5 kg/m2 higher in BMI at all examinations than women without temporal atrophy (p
Notes
Comment In: Neurology. 2005 Jun 14;64(11):1990-1; author reply 1990-115955971
SummaryForPatientsIn: Neurology. 2004 Nov 23;63(10):E19-2015557485
PubMed ID
15557505 View in PubMed
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Brain atrophy evaluated by computed tomography in independent and institutionalized hip fracture patients.

https://arctichealth.org/en/permalink/ahliterature83117
Source
Disabil Rehabil. 2005 Sep 30-Oct 15;27(18-19):1197-202
Publication Type
Article
Author
Sakone R.
Pyhtinen J.
Pääkkö E.
Vähänikkilä H.
Ristiniemi J.
Jalovaara P.
Author Affiliation
Department of Orthopaedic and Trauma Surgery, University Hospital of Oulu, Kajaanintie, Finland.
Source
Disabil Rehabil. 2005 Sep 30-Oct 15;27(18-19):1197-202
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Atrophy
Cerebral Cortex - pathology - radiography
Female
Frontal Lobe - pathology - radiography
Hip Fractures - radiography
Humans
Institutionalization
Male
Middle Aged
Temporal Lobe - pathology - radiography
Tomography, X-Ray Computed
Abstract
PURPOSE: To examine if there is an association between brain computed tomography (CT) findings and place of residence in a series of hip fracture patients. METHOD: The CT scans taken immediately after hip fracture of 215 patients (mean age 81.6 years) living in their own homes or otherwise independently (home-dwelling group) and 95 patients (mean age 82.5 years) permanently institutionalized (institutionalized group) were analysed. RESULTS: The institutionalized patients had significantly more cortical cerebral (frontal, p = 0.004; temporal, p = 0.007; parietal, p
PubMed ID
16278189 View in PubMed
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Cerebral ventricular enlargement relates to neuropsychological measures in unselected AIDS patients.

https://arctichealth.org/en/permalink/ahliterature8522
Source
Acta Neurol Scand. 1989 Jan;79(1):59-62
Publication Type
Article
Date
Jan-1989
Author
J. Jakobsen
C. Gyldensted
B. Brun
P. Bruhn
S. Helweg-Larsen
P. Arlien-Søborg
Author Affiliation
Department of Neuroradiology, Rigshospitalet, Copenhagen, Denmark.
Source
Acta Neurol Scand. 1989 Jan;79(1):59-62
Date
Jan-1989
Language
English
Publication Type
Article
Keywords
Acquired Immunodeficiency Syndrome - pathology - physiopathology - psychology
Adult
Atrophy
Cerebral Cortex - pathology - radiography
Cerebral Ventricles - pathology
Cerebral Ventriculography
Cross-Sectional Studies
Denmark
Dilatation, Pathologic - radiography
Humans
Male
Middle Aged
Neuropsychology
Reaction Time
Tomography, X-Ray Computed
Abstract
In a cross-sectional study of unselected Danish AIDS patients various linear measures of cerebral ventricular size obtained by computed tomography were compared with results of neuropsychological test performances. Third ventricular width as well as right and left septum-caudate distances were enlarged in the patients (P less than 0.01). Of 20 patients 15 had at least one abnormal ventricular measurement. Although only one patient was demented, ventricular size correlated inversely with neuropsychological function (r = -0.61, P less than 0.02). The correlation between ventricular size and variation of the reaction time was even closer (r = 0.74, P less than 0.01). It is concluded that neuroradiological signs of central atrophy often occur in AIDS patients.
PubMed ID
2784608 View in PubMed
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Degradation of the amyloid beta-protein by the novel mitochondrial peptidasome, PreP.

https://arctichealth.org/en/permalink/ahliterature168276
Source
J Biol Chem. 2006 Sep 29;281(39):29096-104
Publication Type
Article
Date
Sep-29-2006
Author
Annelie Falkevall
Nyosha Alikhani
Shashi Bhushan
Pavel F Pavlov
Katrin Busch
Kenneth A Johnson
Therese Eneqvist
Lars Tjernberg
Maria Ankarcrona
Elzbieta Glaser
Author Affiliation
Department of Biochemistry and Biophysics, Stockholm University SE-106 91 Stockholm, Sweden.
Source
J Biol Chem. 2006 Sep 29;281(39):29096-104
Date
Sep-29-2006
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Amino Acid Sequence
Amyloid beta-Peptides - chemistry - metabolism
Animals
Cerebral Cortex - pathology
Humans
Male
Middle Aged
Mitochondria - metabolism
Mitochondrial Proteins - chemistry - physiology
Molecular Sequence Data
Peptides - chemistry
Protein Binding
Rats
Rats, Sprague-Dawley
Sequence Homology, Amino Acid
Serine Endopeptidases - chemistry - physiology
Submitochondrial Particles - chemistry
Abstract
Recently we have identified the novel mitochondrial peptidase responsible for degrading presequences and other short unstructured peptides in mitochondria, the presequence peptidase, which we named PreP peptidasome. In the present study we have identified and characterized the human PreP homologue, hPreP, in brain mitochondria, and we show its capacity to degrade the amyloid beta-protein (Abeta). PreP belongs to the pitrilysin oligopeptidase family M16C containing an inverted zinc-binding motif. We show that hPreP is localized to the mitochondrial matrix. In situ immuno-inactivation studies in human brain mitochondria using anti-hPreP antibodies showed complete inhibition of proteolytic activity against Abeta. We have cloned, overexpressed, and purified recombinant hPreP and its mutant with catalytic base Glu(78) in the inverted zinc-binding motif replaced by Gln. In vitro studies using recombinant hPreP and liquid chromatography nanospray tandem mass spectrometry revealed novel cleavage specificities against Abeta-(1-42), Abeta-(1-40), and Abeta Arctic, a protein that causes increased protofibril formation an early onset familial variant of Alzheimer disease. In contrast to insulin degrading enzyme, which is a functional analogue of hPreP, hPreP does not degrade insulin but does degrade insulin B-chain. Molecular modeling of hPreP based on the crystal structure at 2.1 A resolution of AtPreP allowed us to identify Cys(90) and Cys(527) that form disulfide bridges under oxidized conditions and might be involved in redox regulation of the enzyme. Degradation of the mitochondrial Abeta by hPreP may potentially be of importance in the pathology of Alzheimer disease.
PubMed ID
16849325 View in PubMed
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Effect of apolipoprotein E genotype on Alzheimer's disease neuropathology in a cohort of elderly Norwegians.

https://arctichealth.org/en/permalink/ahliterature213709
Source
Neurosci Lett. 1995 Dec 1;201(1):45-7
Publication Type
Article
Date
Dec-1-1995
Author
C M Morris
R. Benjamin
A. Leake
F K McArthur
J M Candy
P G Ince
A. Torvik
E. Bjertness
J A Edwardson
Author Affiliation
MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne, UK.
Source
Neurosci Lett. 1995 Dec 1;201(1):45-7
Date
Dec-1-1995
Language
English
Publication Type
Article
Keywords
Aged
Alzheimer Disease - genetics - pathology
Apolipoprotein E2
Apolipoprotein E3
Apolipoprotein E4
Apolipoproteins E - genetics
Cerebral Cortex - pathology
Cohort Studies
Genotype
Humans
Neurofibrillary Tangles - pathology
Norway
Abstract
A cohort of elderly Norwegians dying in nursing homes in the Oslo region have been genotyped for the Apolipoprotein E (ApoE) gene. Alzheimer's disease (AD) cortical neuropathology and clinical evidence of dementia were used to assign cases without evidence of other confounding neuropathology. Senile plaque (SP) and neurofibrillary tangle (NFT) densities in frontal, temporal and parietal cortex were then correlated with ApoE genotype to determine any relationship between ApoE genotype and AD pathology. Comparisons with ApoE epsilon 3, epsilon 4 and epsilon 2 allele dosage failed to show any significant effect on cortical SP densities in any cortical area. NFT densities were increased by epsilon 4 allele dosage in the frontal cortex but not in other cortical regions. A reduction was seen in cortical NFT densities with epsilon 2 allele, though again this was not consistently significant in any of the groups. The epsilon 3 allele failed to show any consistent effect on cortical NFT densities. Assessment by individual genotypes showed epsilon 2/3
PubMed ID
8830309 View in PubMed
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Generalized amyloid in a family of Swedish origin. A study of 426 family members in seven generations of a new kinship with neuropathy, nephropathy, and central nervous system involvement.

https://arctichealth.org/en/permalink/ahliterature56074
Source
Ann Intern Med. 1977 Apr;86(4):419-24
Publication Type
Article
Date
Apr-1977
Author
M D Benson
A S Cohen
Source
Ann Intern Med. 1977 Apr;86(4):419-24
Date
Apr-1977
Language
English
Publication Type
Article
Keywords
Adult
Amyloid - metabolism
Amyloidosis - complications - diagnosis - genetics
Central Nervous System Diseases - etiology
Cerebral Cortex - pathology
Gastrointestinal Diseases - etiology
Heart Diseases - etiology
Humans
Kidney Diseases - etiology
Male
Meninges - pathology
Myocardium - pathology
Pedigree
Peripheral Nervous System Diseases - etiology
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Sural Nerve - pathology
Sweden - ethnology
United States
Abstract
We report a new kinship with systemic amyloid presenting as peripheral neuropathy in the fourth and fifth decades of life. A progressive sensory and motor loss starting in the lower extremities occurs from this disease, and there is subsequent renal, cardiac, gastrointestinal, ocular, and cutaneous involvement. Histologic studies show that amyloid deposition is mainly in connective tissue structures; there is an unusual infiltration of the meninges and central nervous system. Review of records of 426 family members in seven generations showed that this disease is inherited as an autosomal dominant. The absence of immunoglobulin disorders in two affected family members studied in depth suggests that this is not the primary type of amyloid in which the deposits are composed of fragments of immunoglobulin light chains. Similarly the absence of elevated levels of protein SAA (the serum precursor of secondary amyloid) suggests that this is not a secondary form of amyloid.
PubMed ID
192115 View in PubMed
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Late-onset Alzheimer disease genetic variants in posterior cortical atrophy and posterior AD.

https://arctichealth.org/en/permalink/ahliterature104624
Source
Neurology. 2014 Apr 22;82(16):1455-62
Publication Type
Article
Date
Apr-22-2014
Author
Minerva M Carrasquillo
Qurat ul Ain Khan
Melissa E Murray
Siddharth Krishnan
Jeremiah Aakre
V Shane Pankratz
Thuy Nguyen
Li Ma
Gina Bisceglio
Ronald C Petersen
Steven G Younkin
Dennis W Dickson
Bradley F Boeve
Neill R Graff-Radford
Nilüfer Ertekin-Taner
Author Affiliation
From the Departments of Neuroscience (M.M.C., M.E.M., S.K., T.N., L.M., G.B., S.G.Y., D.W.D., N.E.-T.) and Neurology (Q.u.A.K., N.R.G.-R., N.E.-T.), Mayo Clinic Florida, Jacksonville; and Departments of Biostatistics (J.A., V.S.P.) and Neurology (R.C.P., B.F.B.), Mayo Clinic Minnesota, Rochester.
Source
Neurology. 2014 Apr 22;82(16):1455-62
Date
Apr-22-2014
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alzheimer Disease - diagnosis - epidemiology - genetics
Atrophy
Cerebral Cortex - pathology
Cerebral Ventricles - pathology
Comorbidity
Cross-Sectional Studies
Female
Genetic Variation - genetics
Humans
Male
Neurologic Examination
Neuropsychological Tests
Sweden
Tomography, X-Ray Computed
Abstract
To investigate association of genetic risk factors for late-onset Alzheimer disease (LOAD) with risk of posterior cortical atrophy (PCA), a syndrome of visual impairment with predominant Alzheimer disease (AD) pathology in posterior cortical regions, and with risk of "posterior AD" neuropathology.
We assessed 81 participants with PCA diagnosed clinically and 54 with neuropathologic diagnosis of posterior AD vs 2,523 controls for association with 11 significant single nucleotide polymorphisms (SNPs) from published LOAD risk genome-wide association studies.
There was highly significant association with APOE e4 and increased risk of PCA (p = 0.0003, odds ratio [OR] = 3.17) and posterior AD (p = 1.11 × 10(-17), OR = 6.43). No other locus was significant after corrections for multiple testing, although rs11136000 near CLU (p = 0.019, OR = 0.60) and rs744373 near BIN1 (p = 0.025, OR = 1. 63) associated nominally significantly with posterior AD, and rs3851179 at the PICALM locus had significant association with PCA (p = 0.0003, OR = 2.84). ABCA7 locus SNP rs3764650, which was also tested under the recessive model because of Hardy-Weinberg disequilibrium, also had nominally significant association with PCA risk. The direction of association at APOE, CLU, and BIN1 loci was the same for participants with PCA and posterior AD. The effects for all SNPs, except rs3851179, were consistent with those for LOAD risk.
We identified a significant effect for APOE and nominate CLU, BIN1, and ABCA7 as additional risk loci for PCA and posterior AD. Our findings suggest that at least some of the genetic risk factors for LOAD are shared with these atypical conditions and provide effect-size estimates for their future genetic studies.
PubMed ID
24670887 View in PubMed
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Lethal arthrogryposis in Finland--a clinico-pathological study of 83 cases during thirteen years.

https://arctichealth.org/en/permalink/ahliterature59348
Source
Neuropediatrics. 1994 Dec;25(6):308-15
Publication Type
Article
Date
Dec-1994
Author
K. Vuopala
J. Leisti
R. Herva
Author Affiliation
Department of Pathology, University of Oulu, Finland.
Source
Neuropediatrics. 1994 Dec;25(6):308-15
Date
Dec-1994
Language
English
Publication Type
Article
Keywords
Arthrogryposis - epidemiology - pathology
Autopsy
Cerebral Cortex - pathology - ultrastructure
Female
Fetal Death
Finland - epidemiology
Gestational Age
Humans
Infant, Newborn
Male
Muscle, Skeletal - pathology - ultrastructure
Research Support, Non-U.S. Gov't
Retrospective Studies
Abstract
Eighty-three cases of multiple congenital joint contractures, i.e., arthrogryposis, which were related with either a stillborn fetus, a termination of pregnancy following prenatal diagnosis or death within 28 days postnatally, were studied. Sixty-seven cases were neurogenic in origin, including forty-one with the lethal congenital contracture syndrome (LCCS, McKusick 253310), fifteen with milder anterior horn cell involvement, and ten with dysgenesis and degeneration of the CNS. Congenital muscular dystrophy was seen in two cases and nemaline myopathy in one case. A non-neuromuscular basis was established in ten cases, and the cause remained obscure in three cases. Apart from the autosomal recessive LCCS, the fifteen cases with anterior horn cell involvement made up a uniform clinico-pathological entity. In two families this disease recurred twice, and autosomal recessive inheritance is therefore likely. Recurrence was also seen twice in a family with central nervous system degeneration and in another with the oligohydramnios sequence. There are apparently several recessively inherited entities among the arthrogryposis phenotype. A careful clinical study and a neuropathological examination are essential for estimating the recurrence risk.
PubMed ID
7770128 View in PubMed
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No progressive brain changes during a 1-year follow-up of patients with first-episode psychosis.

https://arctichealth.org/en/permalink/ahliterature276617
Source
Psychol Med. 2016 Feb;46(3):589-98
Publication Type
Article
Date
Feb-2016
Author
U K Haukvik
C B Hartberg
S. Nerland
K N Jørgensen
E H Lange
C. Simonsen
R. Nesvåg
A M Dale
O A Andreassen
I. Melle
I. Agartz
Source
Psychol Med. 2016 Feb;46(3):589-98
Date
Feb-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Antipsychotic Agents - therapeutic use
Bipolar Disorder - drug therapy - pathology
Case-Control Studies
Cerebral Cortex - pathology
Disease Progression
Female
Follow-Up Studies
Humans
Linear Models
Longitudinal Studies
Magnetic Resonance Imaging
Male
Middle Aged
Norway
Psychotic Disorders - drug therapy - pathology
Schizophrenia - drug therapy - pathology
Young Adult
Abstract
First-episode psychosis (FEP) patients show structural brain abnormalities. Whether the changes are progressive or not remain under debate, and the results from longitudinal magnetic resonance imaging (MRI) studies are mixed. We investigated if FEP patients showed a different pattern of regional brain structural change over a 1-year period compared with healthy controls, and if putative changes correlated with clinical characteristics and outcome.
MRIs of 79 FEP patients [SCID-I-verified diagnoses: schizophrenia, psychotic bipolar disorder, or other psychoses, mean age 27.6 (s.d. = 7.7) years, 66% male] and 82 healthy controls [age 29.3 (s.d. = 7.2) years, 66% male] were acquired from the same 1.5 T scanner at baseline and 1-year follow-up as part of the Thematically Organized Psychosis (TOP) study, Oslo, Norway. Scans were automatically processed with the longitudinal stream in FreeSurfer that creates an unbiased within-subject template image. General linear models were used to analyse longitudinal change in a wide range of subcortical volumes and detailed thickness and surface area estimates across the entire cortex, and associations with clinical characteristics.
FEP patients and controls did not differ significantly in annual percentage change in cortical thickness or area in any cortical region, or in any of the subcortical structures after adjustment for multiple comparisons. Within the FEP group, duration of untreated psychosis, age at illness onset, antipsychotic medication use and remission at follow-up were not related to longitudinal brain change.
We found no significant longitudinal brain changes over a 1-year period in FEP patients. Our results do not support early progressive brain changes in psychotic disorders.
PubMed ID
26526001 View in PubMed
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21 records – page 1 of 3.