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000139228 0247_ $$2doi$$a10.1186/s40478-017-0437-5
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000139228 037__ $$aDZNE-2020-05550
000139228 041__ $$aEnglish
000139228 082__ $$a610
000139228 1001_ $$0P:(DE-HGF)0$$aDavidson, Yvonne S$$b0
000139228 245__ $$aHeterogeneous ribonuclear protein A3 (hnRNP A3) is present in dipeptide repeat protein containing inclusions in Frontotemporal Lobar Degeneration and Motor Neurone disease associated with expansions in C9orf72 gene.
000139228 260__ $$aLondon$$bBiomed Central$$c2017
000139228 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2017-04-21
000139228 264_1 $$2Crossref$$3print$$bSpringer Science and Business Media LLC$$c2017-12-01
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000139228 520__ $$aFrontotemporal Lobar Degeneration (FTLD) encompasses certain related neurodegenerative disorders which alter behaviour, personality and language. Heterogeneous ribonuclear proteins (hnRNPs) maintain RNA metabolism and changes in their function may underpin the pathogenesis of FTLD. Immunostaining for hnRNP A1, A2/B1 and A3 was performed on sections of temporal cortex with hippocampus from 61 patients with FTLD, stratified by pathological hallmarks into FTLD-tau and FTLD-TDP type A, B and C subtypes, and by genetics into patients with C9orf72 expansions, MAPT or GRN mutations, or those without known mutation. Four patients with Motor Neurone Disease (MND) with C9orf72 expansions and 10 healthy controls were also studied. Semi-quantitative analysis assessed hnRNP staining intensity in dentate gyrus (DG) and CA4 region of hippocampus, and temporal cortex (Tcx) in the different pathological and genetic groups.Immunostaining for hnRNP A1, A2/B1 and A3 revealed no consistent changes in pattern or amount of physiological staining across any of the pathological or genetic groups. No immunostaining of any inclusions resembling TDP-43 immunoreactive neuronal cytoplasmic inclusions or dystrophic neurites, was seen in either Tcx or DG of the hippocampus in any of the FTLD cases investigated for hnRNP A1, A2/B1 and A3. However, immunostaining for hnRNP A3 showed that inclusion bodies, resembling those TDP-43 negative, p62-immunopositive structures containing dipeptide repeat proteins (DPR) were variably observed in hippocampus and cerebellum. The proportion of cases showing hnRNP A3-immunoreactive DPR, and the number of hnRNP A3-positive inclusions within cases, was significantly greater in DG than in cells of CA4 region and cerebellum, but the latter was significantly less in all three regions compared to that detected by p62 immunostaining.
000139228 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
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000139228 650_7 $$2NLM Chemicals$$aC9orf72 Protein
000139228 650_7 $$2NLM Chemicals$$aC9orf72 protein, human
000139228 650_7 $$2NLM Chemicals$$aDNA-Binding Proteins
000139228 650_7 $$2NLM Chemicals$$aGRN protein, human
000139228 650_7 $$2NLM Chemicals$$aHNRNPA3 protein, human
000139228 650_7 $$2NLM Chemicals$$aHeterogeneous Nuclear Ribonucleoprotein A1
000139228 650_7 $$2NLM Chemicals$$aHeterogeneous-Nuclear Ribonucleoprotein Group A-B
000139228 650_7 $$2NLM Chemicals$$aIntercellular Signaling Peptides and Proteins
000139228 650_7 $$2NLM Chemicals$$aMAPT protein, human
000139228 650_7 $$2NLM Chemicals$$aProgranulins
000139228 650_7 $$2NLM Chemicals$$aTDP-43 protein, human
000139228 650_7 $$2NLM Chemicals$$ahnRNP A2
000139228 650_7 $$2NLM Chemicals$$atau Proteins
000139228 650_2 $$2MeSH$$aAged
000139228 650_2 $$2MeSH$$aAged, 80 and over
000139228 650_2 $$2MeSH$$aC9orf72 Protein: genetics
000139228 650_2 $$2MeSH$$aCerebellum: metabolism
000139228 650_2 $$2MeSH$$aCerebellum: pathology
000139228 650_2 $$2MeSH$$aDNA Repeat Expansion
000139228 650_2 $$2MeSH$$aDNA-Binding Proteins: metabolism
000139228 650_2 $$2MeSH$$aFemale
000139228 650_2 $$2MeSH$$aFrontotemporal Lobar Degeneration: genetics
000139228 650_2 $$2MeSH$$aFrontotemporal Lobar Degeneration: metabolism
000139228 650_2 $$2MeSH$$aFrontotemporal Lobar Degeneration: pathology
000139228 650_2 $$2MeSH$$aHeterogeneous Nuclear Ribonucleoprotein A1: metabolism
000139228 650_2 $$2MeSH$$aHeterogeneous-Nuclear Ribonucleoprotein Group A-B: metabolism
000139228 650_2 $$2MeSH$$aHippocampus: metabolism
000139228 650_2 $$2MeSH$$aHippocampus: pathology
000139228 650_2 $$2MeSH$$aHumans
000139228 650_2 $$2MeSH$$aInclusion Bodies: metabolism
000139228 650_2 $$2MeSH$$aInclusion Bodies: pathology
000139228 650_2 $$2MeSH$$aIntercellular Signaling Peptides and Proteins: genetics
000139228 650_2 $$2MeSH$$aMale
000139228 650_2 $$2MeSH$$aMiddle Aged
000139228 650_2 $$2MeSH$$aMotor Neuron Disease: genetics
000139228 650_2 $$2MeSH$$aMotor Neuron Disease: metabolism
000139228 650_2 $$2MeSH$$aMotor Neuron Disease: pathology
000139228 650_2 $$2MeSH$$aProgranulins
000139228 650_2 $$2MeSH$$aTemporal Lobe: metabolism
000139228 650_2 $$2MeSH$$aTemporal Lobe: pathology
000139228 650_2 $$2MeSH$$atau Proteins: genetics
000139228 7001_ $$0P:(DE-HGF)0$$aFlood, Louis$$b1
000139228 7001_ $$0P:(DE-HGF)0$$aRobinson, Andrew C$$b2
000139228 7001_ $$0P:(DE-HGF)0$$aNihei, Yoshihiro$$b3
000139228 7001_ $$0P:(DE-HGF)0$$aMori, Kohji$$b4
000139228 7001_ $$0P:(DE-HGF)0$$aRollinson, Sara$$b5
000139228 7001_ $$0P:(DE-HGF)0$$aRichardson, Anna$$b6
000139228 7001_ $$0P:(DE-HGF)0$$aBenson, Bridget C$$b7
000139228 7001_ $$0P:(DE-HGF)0$$aJones, Matthew$$b8
000139228 7001_ $$0P:(DE-HGF)0$$aSnowden, Julie S$$b9
000139228 7001_ $$0P:(DE-HGF)0$$aPickering-Brown, Stuart$$b10
000139228 7001_ $$0P:(DE-2719)2202037$$aHaass, Christian$$b11$$udzne
000139228 7001_ $$0P:(DE-HGF)0$$aLashley, Tammaryn$$b12
000139228 7001_ $$0P:(DE-HGF)0$$aMann, David M A$$b13$$eCorresponding author
000139228 77318 $$2Crossref$$3journal-article$$a10.1186/s40478-017-0437-5$$b : Springer Science and Business Media LLC, 2017-04-21$$n1$$p31$$tActa Neuropathologica Communications$$v5$$x2051-5960$$y2017
000139228 773__ $$0PERI:(DE-600)2715589-4$$a10.1186/s40478-017-0437-5$$gVol. 5, no. 1, p. 31$$n1$$p31$$q5:1<31$$tActa Neuropathologica Communications$$v5$$x2051-5960$$y2017
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