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Age-related changes in HSP25 expression in basal ganglia and cortex of F344/BN rats.

https://arctichealth.org/en/permalink/ahliterature98106
Source
Neurosci Lett. 2010 Mar 19;472(2):90-3
Publication Type
Article
Date
Mar-19-2010
Author
Anisha A Gupte
Jill K Morris
Hongyu Zhang
Gregory L Bomhoff
Paige C Geiger
John A Stanford
Author Affiliation
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, United States.
Source
Neurosci Lett. 2010 Mar 19;472(2):90-3
Date
Mar-19-2010
Language
English
Publication Type
Article
Keywords
Age Factors
Animals
Basal Ganglia - metabolism
Cerebral Cortex - metabolism
HSP27 Heat-Shock Proteins - biosynthesis
HSP72 Heat-Shock Proteins - biosynthesis
Phosphorylation
Rats
Rats, Inbred BN
Rats, Inbred F344
p38 Mitogen-Activated Protein Kinases - biosynthesis
Abstract
Normal aging is associated with chronic oxidative stress. In the basal ganglia, oxidative stress may contribute to the increased risk of Parkinson's disease in the elderly. Neurons are thought to actively utilize compensatory defense mechanisms, such as heat shock proteins (HSPs), to protect from persisting stress. Despite their protective role, little is known about HSP expression in the aging basal ganglia. The purpose of this study was to examine HSP expression in striatum, substantia nigra, globus pallidus and cortex in 6-, 18- and 30-month-old Fischer 344/Brown Norway rats. We found robust age-related increases in phosphorylated and total HSP25 in each brain region studied. Conversely, HSP72 (the inducible form of HSP70) was reduced with age, but only in the striatum. p38 MAPK, a protein implicated in activating HSP25, did not change with age, nor did HSC70 (the constitutive form of HSP70), or HSP60. These results suggest that HSP25 is especially responsive to age-related stress in the basal ganglia.
PubMed ID
20144690 View in PubMed
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Amyloid and tau proteins in cortical brain biopsy and Alzheimer's disease.

https://arctichealth.org/en/permalink/ahliterature139810
Source
Ann Neurol. 2010 Oct;68(4):446-53
Publication Type
Article
Date
Oct-2010
Author
Ville Leinonen
Anne M Koivisto
Sakari Savolainen
Jaana Rummukainen
Juuso N Tamminen
Tomi Tillgren
Sannakaisa Vainikka
Okko T Pyykkö
Juhani Mölsä
Mikael Fraunberg
Tuula Pirttilä
Juha E Jääskeläinen
Hilkka Soininen
Jaakko Rinne
Irina Alafuzoff
Author Affiliation
Department of Neurosurgery, Kuopio University Hospital, Kuopio, Finland. ville.leinonen@kuh.fi
Source
Ann Neurol. 2010 Oct;68(4):446-53
Date
Oct-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Alzheimer Disease - complications - pathology
Amyloid beta-Peptides - metabolism
Biopsy - methods
Cerebral Cortex - metabolism
Cognition Disorders - etiology
Female
Finland
Humans
Logistic Models
Longitudinal Studies
Male
Middle Aged
Psychiatric Status Rating Scales
Retrospective Studies
Sensitivity and specificity
tau Proteins - metabolism
Abstract
Amyloid-ß(Aß) aggregates are presumed to be found in the brain at an early stage of Alzheimer's disease (AD) but have seldom been assessed by brain biopsy during life in often elderly patients.
Between 1991 and 2006 we evaluated 468 patients with suspected normal pressure hydrocephalus with intraventricular pressure monitoring and a right frontal cortical biopsy sample immunostained for Aß and hyperphosphorylated tau (HPt). Adequate samples and the clinical follow-up data until death or the end of 2008, available in 433 cases, were reviewed for the clinical signs of dementia, including AD. Logistic regression analysis was used to analyze whether Aß and/or HPt in the biopsy samples obtained during life predicted development of cognitive impairment, in particular, AD.
Of the 433 frontal cortical samples, 42 (10%) displayed both Aß and HPt, 144 (33%) Aß only, and 247 (57%) neither Aß nor HPt. In a median follow-up time of 4.4 years, 94 patients (22%) developed clinical AD. The presence of both Aß and HPt was strongly associated (odds ratio [OR], 68.2; 95% confidence interval [CI], 22.1-210) and Aß alone significantly associated (OR, 10.8; 95% CI, 4.9-23.8) with the clinical diagnosis of AD.
This is the largest follow-up study of patients assessed for the presence of Aß and HPt in frontal cortical brain biopsy samples. 1) The presence of Aß and HPt spoke strongly for the presence or later development of clinical AD; 2) Aß alone was suggestive of AD; and 3) the absence of Aß and HPt spoke against a later clinical diagnosis of AD.
PubMed ID
20976765 View in PubMed
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Anticholinergic drug use, serum anticholinergic activity, and adverse drug events among older people: a population-based study.

https://arctichealth.org/en/permalink/ahliterature115704
Source
Drugs Aging. 2013 May;30(5):321-30
Publication Type
Article
Date
May-2013
Author
Pasi Lampela
Piia Lavikainen
J Arturo Garcia-Horsman
J Simon Bell
Risto Huupponen
Sirpa Hartikainen
Author Affiliation
Kuopio Research Centre of Geriatric Care, University of Eastern Finland, Kuopio Campus, P.O. Box 1627, 70211 Kuopio, Finland. Pasi.Lampela@uef.fi
Source
Drugs Aging. 2013 May;30(5):321-30
Date
May-2013
Language
English
Publication Type
Article
Keywords
Activities of Daily Living
Aged
Aged, 80 and over
Animals
Cerebral Cortex - metabolism
Cholinergic Antagonists - adverse effects - blood - therapeutic use
Depression - prevention & control
Female
Finland
Geriatric Assessment
Humans
Male
Mental Status Schedule
Pulmonary Disease, Chronic Obstructive - drug therapy
Rats
Rats, Wistar
Urinary Bladder, Overactive - drug therapy
Abstract
The serum anticholinergic activity (SAA) assay has been used to quantify patients' anticholinergic load. In addition, several ranked lists of anticholinergic drugs have been developed to assess anticholinergic drug burden.
This study investigated whether SAA assay results and scores from three ranked lists of anticholinergic drugs (Carnahan's Anticholinergic Drug Scale, Rudolph's Anticholinergic Risk Scale, and Chew's list) are associated with anticholinergic adverse drug events (ADEs) in older people.
We analyzed data from participants in the population-based Geriatric Multidisciplinary Good Care of the Elderly Study in Kuopio, Finland (n = 621). Demographic, diagnostic, and drug use data were collected during standardized interviews and verified from medical records. Vision, functional capacity, cognition, and mood were assessed using validated techniques. The SAA was measured from blood samples.
The SAA was not associated with anticholinergic ADEs. Anticholinergic drug burden computed using each of the three lists was inversely associated with short-distance vision (p 
Notes
Comment In: J Urol. 2014 Aug;192(2):49025035017
PubMed ID
23475596 View in PubMed
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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
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Chronic administration of imipramine normalizes decreased sexual motivation and increased predisposition to catalepsy induced by propylthiouracil in rats.

https://arctichealth.org/en/permalink/ahliterature89440
Source
Neurosci Behav Physiol. 2009 May;39(4):409-15
Publication Type
Article
Date
May-2009
Author
Tikhonova M A
Amstislavskaya T G
Kulikov A V
Author Affiliation
Behavioral Neurogenomics Laboratory, Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences, Novosibirsk, Russia. mar-a-tikh@mail.ru
Source
Neurosci Behav Physiol. 2009 May;39(4):409-15
Date
May-2009
Language
English
Publication Type
Article
Keywords
Animals
Antidepressive Agents, Tricyclic - therapeutic use
Antithyroid Agents
Catalepsy - chemically induced - drug therapy - psychology
Cerebral Cortex - metabolism
Imipramine - therapeutic use
Male
Propylthiouracil
Rats
Rats, Wistar
Receptor, Serotonin, 5-HT2A - metabolism
Sexual Behavior, Animal - drug effects
Sexual Dysfunction, Physiological - chemically induced - drug therapy
Abstract
Thyroxine synthesis inhibitors increase the predisposition to catalepsy and decrease sexual motivation and the amplitude of the acoustic startle reflex in rats. The sensitivity of these behavioral changes to antidepressants remains uncertain. Chronic administration of the classical tricyclic antidepressant imipramine (15 mg/kg, 21 days) prevented the appearance of high sensitivity to catalepsy and the decrease in sexual motivation in Wistar rats given propylthiouracil (50 mg/liter, 28 days), without altering the amplitude of the startle reflex. Normalization of behavior in response to imipramine was not associated with changes in movement activity in the open field test or the animals' body weight. There was also no change in the expression of the 5-HT2A serotonin receptor gene in the frontal cortex. The model of propylthiouracilinduced catalepsy with reduced sexual motivation in rats has potential for studying the role of thyroid abnormalities in the development of depression and the mechanisms of action of antidepressants.
PubMed ID
19340585 View in PubMed
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[Effect of cross-fostering on catalepsy and the brain monoamine level in rat offspring prone to catalepsy and in the control strain]

https://arctichealth.org/en/permalink/ahliterature10140
Source
Ross Fiziol Zh Im I M Sechenova. 2001 Jul;87(7):918-25
Publication Type
Article
Date
Jul-2001
Author
V G Kolpakov
T A Alekhina
T G Amstislavskaia
V F Chugui
N N Barykina
S Ia Amstislavskii
Author Affiliation
Institute of Cytology and Genetics, Russian Acad. Sci., Siberian Branch, Russia, 630090, Novosibirsk, Pr. Lavrentyeva, 10.
Source
Ross Fiziol Zh Im I M Sechenova. 2001 Jul;87(7):918-25
Date
Jul-2001
Language
Russian
Publication Type
Article
Keywords
Animals
Animals, Newborn
Biogenic Monoamines - metabolism
Brain - metabolism
Catalepsy - genetics - metabolism - psychology
Cerebral Cortex - metabolism
Comparative Study
Corpus Striatum - metabolism
Dopamine - metabolism
English Abstract
Female
Genotype
Hypothalamus - metabolism
Male
Maternal Behavior
Medulla Oblongata - metabolism
Norepinephrine - metabolism
Rats
Rats, Wistar
Selection (Genetics)
Serotonin - metabolism
Abstract
Duration of cataleptic reactions in male rats of Wistar and GC strains depended both on the genotype and on the type of rearing: it was longer in the GC rats than in the Wistar ones. In the GC males reared by Wistar foster mothers this parameter was smaller than in the control GC but higher than in Wistar rats. The NA content was significantly lower in the GC cortex, hypothalamus and striatum, and the level of serotonin and 5-HIAA was lower in cortex of the GC as compared with Wistar rats. The cross-fostering affected monoamine content in some brain structures. On the whole, serotonin, DA and NA systems of the GC rats proved to be more susceptible to stress caused by cross-fostering than those of the Wistar rats. The cross-fostering diminished interstrain differences in the NA level in cortex, striatum, and hypothalamus.
PubMed ID
11575125 View in PubMed
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Evaluation of oxidative status and depression-like responses in Brown Norway rats with acute myeloid leukemia.

https://arctichealth.org/en/permalink/ahliterature89746
Source
Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):596-604
Publication Type
Article
Date
Jun-15-2009
Author
Papiez Monika A
Dybala Malgorzata
Sowa-Kucma Magdalena
Krzysciak Wirginia
Taha Hevidar
Jozkowicz Alicja
Nowak Gabriel
Author Affiliation
Department of Cytobiology & Histochemistry, Faculty of Pharmacy, Jagiellonian University, Krakow, Poland. mfpapiez@cyf-kr.edu.pl
Source
Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):596-604
Date
Jun-15-2009
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Animals
Behavior, Animal
Biliverdine - genetics - metabolism
Body Weight
Cerebral Cortex - metabolism
Depression - etiology
Disease Models, Animal
Ferritins - genetics - metabolism
Glutathione - metabolism
Heme Oxygenase (Decyclizing) - genetics - metabolism
Hippocampus - metabolism
Leukemia, Myeloid, Acute - complications - pathology
Lipid Peroxidation - physiology
Male
Motor Activity - physiology
Oxidative Stress - physiology
Protein Binding - physiology
Radioligand Assay - methods
Rats
Rats, Inbred BN
Receptors, Biogenic Amine - metabolism
Spectrophotometry
Spleen - metabolism
Swimming
Abstract
It has been proved that oxidative stress increases when leukemia is accompanied by depression. This fact may indicate the role of oxidative stress in the development of depression in cancer patients. The aim of this study was to determine whether the acute myeloid leukemia of Brown Norway rats, which is accompanied by oxidative stress, evoked behavioral and receptor changes resembling alterations characteristic of rat models of depression. The rats were divided into two groups: leukemic rats and healthy control. Leukemia was induced through intraperitoneal injection of 10(7) promyelocytic leukemia cells to the Brown Norway rats. Depression-like behavior was evaluated in the forced swim test at 30 or 34 days after leukemic cells injection. The rats were killed after the evaluation and the spleen, brain cortex and hippocampus were excised. The red-ox state was assessed in homogenates of tissues by measuring total glutathione (GSH) content, the ferric ion reducing ability of plasma (FRAP) level, expression of heme oxygenase-1 (HO-1), biliverdin reductase (BvR) and ferritin mRNA, superoxide dismutase (SOD) activity, as well as malondialdehyde (MDA) concentration. Radioligand binding assay was used to assess of the effect of leukemia on cortical receptors. Leukemic cells were identified using RM-124 antibody by FACS Calibur flow cytometry. Leukemia influenced locomotory activity as well as forced swim test behavior in a 34-day series of experiments. Signs of oxidative stress in leukemic rats were observed in each examined stage of leukemia development. The FRAP values and glutathione contents, were significantly lowered whereas HO-1 mRNA expression, and malonodialdehyde concentrations were significantly increased in the spleen and brain structures of leukemic rats in comparison with the healthy controls. A significant increase in the potency of glycine to displace [(3)H]L-689,560 from the strychnine-insensitive glycine site of the N-methyl-D-aspartic (NMDA) receptors receptor complex in cortical homogenates of the leukemic rats in 30- and 34-day experimental series was observed in comparison with the control. Upregulation of 5-HT(2A) receptors was observed in rat cortex after 30 days of leukemia development but not in 34-days series compared with the control. It is concluded that disturbances in antioxidant system in brain cortex were accompanied by an activation of glycine sites of the NMDA receptor complex, regardless of stage of leukemia development, which are characteristic of model of depression. Findings of our study demonstrate the link between glutamatergic activity, oxidative stress and leukemia.
PubMed ID
19268504 View in PubMed
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Gene-based analysis of regionally enriched cortical genes in GWAS data sets of cognitive traits and psychiatric disorders.

https://arctichealth.org/en/permalink/ahliterature126517
Source
PLoS One. 2012;7(2):e31687
Publication Type
Article
Date
2012
Author
Kari M Ersland
Andrea Christoforou
Christine Stansberg
Thomas Espeseth
Manuel Mattheisen
Morten Mattingsdal
Gudmundur A Hardarson
Thomas Hansen
Carla P D Fernandes
Sudheer Giddaluru
René Breuer
Jana Strohmaier
Srdjan Djurovic
Markus M Nöthen
Marcella Rietschel
Astri J Lundervold
Thomas Werge
Sven Cichon
Ole A Andreassen
Ivar Reinvang
Vidar M Steen
Stephanie Le Hellard
Author Affiliation
Dr E Martens Research Group for Biological Psychiatry, Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Source
PLoS One. 2012;7(2):e31687
Date
2012
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Animals
Bipolar Disorder - genetics
Case-Control Studies
Cerebral Cortex - metabolism
Cognition - physiology
Cognition Disorders - genetics
Female
Frontal Lobe - pathology
Genome-Wide Association Study
Humans
Male
Mental Disorders - genetics
Middle Aged
Models, Genetic
Norway
Occipital Lobe - pathology
Rats
Schizophrenia - genetics
Temporal Lobe - pathology
Abstract
Despite its estimated high heritability, the genetic architecture leading to differences in cognitive performance remains poorly understood. Different cortical regions play important roles in normal cognitive functioning and impairment. Recently, we reported on sets of regionally enriched genes in three different cortical areas (frontomedial, temporal and occipital cortices) of the adult rat brain. It has been suggested that genes preferentially, or specifically, expressed in one region or organ reflect functional specialisation. Employing a gene-based approach to the analysis, we used the regionally enriched cortical genes to mine a genome-wide association study (GWAS) of the Norwegian Cognitive NeuroGenetics (NCNG) sample of healthy adults for association to nine psychometric tests measures. In addition, we explored GWAS data sets for the serious psychiatric disorders schizophrenia (SCZ) (n = 3 samples) and bipolar affective disorder (BP) (n = 3 samples), to which cognitive impairment is linked.
At the single gene level, the temporal cortex enriched gene RAR-related orphan receptor B (RORB) showed the strongest overall association, namely to a test of verbal intelligence (Vocabulary, P = 7.7E-04). We also applied gene set enrichment analysis (GSEA) to test the candidate genes, as gene sets, for enrichment of association signal in the NCNG GWAS and in GWASs of BP and of SCZ. We found that genes differentially expressed in the temporal cortex showed a significant enrichment of association signal in a test measure of non-verbal intelligence (Reasoning) in the NCNG sample.
Our gene-based approach suggests that RORB could be involved in verbal intelligence differences, while the genes enriched in the temporal cortex might be important to intellectual functions as measured by a test of reasoning in the healthy population. These findings warrant further replication in independent samples on cognitive traits.
Notes
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PubMed ID
22384057 View in PubMed
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[The state of the glial intermediate filaments and learning in rats with experimental diabetes]

https://arctichealth.org/en/permalink/ahliterature47289
Source
Fiziol Zh. 2004;50(1):85-90
Publication Type
Article
Date
2004
Author
V S Nedzvets'kyi
Author Affiliation
Dnepropetrovsk National University.
Source
Fiziol Zh. 2004;50(1):85-90
Date
2004
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Behavior, Animal - physiology
Cerebellum - metabolism
Cerebral Cortex - metabolism
Diabetes Mellitus, Experimental - metabolism - physiopathology
English Abstract
Glial Fibrillary Acidic Protein - biosynthesis
Hippocampus - metabolism
Immunoblotting
Learning - physiology
Male
Rats
Rats, Wistar
Abstract
The effect of streptozotocin-induced diabetes on glial intermediate filament and behavioral reactions of rats was investigated. The water Morris test shows cognitive deficit in diabetic rats. The results of an immunoblot show both an increase in GFAP degradation and an increase in common GFAP amount in the brain of diabetic rats. The observations presented here suggest that diabetes induces the changes in activity of GFAP-positive glial cells. Such glial cells may be considered a key element in plasticity of nervous system. These results suggest that the impairment of learning and memory is accompanied by glial cytoskeletal reconstruction.
PubMed ID
14965058 View in PubMed
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A transgenic rat expressing human APP with the Swedish Alzheimer's disease mutation.

https://arctichealth.org/en/permalink/ahliterature77683
Source
Biochem Biophys Res Commun. 2007 Jul 6;358(3):777-82
Publication Type
Article
Date
Jul-6-2007
Author
Folkesson Ronnie
Malkiewicz Katarzyna
Kloskowska Ewa
Nilsson Tatjana
Popova Elena
Bogdanovic Nenad
Ganten Ursula
Ganten Detlev
Bader Michael
Winblad Bengt
Benedikz Eirikur
Author Affiliation
Karolinska Institutet, Department of Neurobiology, Caring Sciences and Society, Novum, 141 86 Stockholm, Sweden.
Source
Biochem Biophys Res Commun. 2007 Jul 6;358(3):777-82
Date
Jul-6-2007
Language
English
Publication Type
Article
Keywords
Alzheimer Disease - genetics - metabolism
Amyloid - biosynthesis - chemistry - metabolism
Animals
Animals, Genetically Modified
Brain - metabolism
Cerebellum - metabolism
Cerebral Cortex - metabolism
Genetic Techniques
Hippocampus - metabolism
Humans
Mutation
Presenilin-1 - genetics
Rats
Sweden
tau Proteins - metabolism
Abstract
In recent years, transgenic mice have become valuable tools for studying mechanisms of Alzheimer's disease (AD). With the aim of developing an animal model better for memory and neurobehavioural testing, we have generated a transgenic rat model of AD. These animals express human amyloid precursor protein (APP) containing the Swedish AD mutation. The highest level of expression in the brain is found in the cortex, hippocampus, and cerebellum. Starting after the age of 15 months, the rats show increased tau phosphorylation and extracellular Abeta staining. The Abeta is found predominantly in cerebrovascular blood vessels with very rare diffuse plaques. We believe that crossing these animals with mutant PS1 transgenic rats will result in accelerated plaque formation similar to that seen in transgenic mice.
PubMed ID
17506994 View in PubMed
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