Clemes Grün, Hüftbild

Signatur des Originals: S 36/F04265

Clemes Grün, Beatrice Kernic, Alfred Hauck, Szenenfoto, Gruppenbildnis, in: Heinrich Reinhardt: Das süße Mädel

Signatur des Originals: S 36/F04267

Clemens Grün, Rollenbild

Signatur des Originals: S 36/F04268

Clemens Grün, Alfred Hauck, Heinrich Hensel, Hermann Schramm {[u.a.], Rollenbild, Gruppenbildnis

Signatur des Originals: S 36/F06343

Clemens Grün, Szenenfoto

Signatur des Originals: S 36/F08705

Clemens Grün, Brustbild, Profil

Signatur des Originals: S 36/F08706

Friederike Christine Christiane Grün, Brustbild

Signatur des Originals: S 36/G00058

Friederike Christine Christiane Grün, Brustbild

Signatur des Originals: S 36/G01023

Friederike Christine Christiane Grün, Brustbild

Signatur des Originals: S 36/G01024

Franz Grillparzer, Eduard von Bauernfeld, Anastasius Grün, Franz Stelzhammer, Johann Ludwig Deinhardstein {[u.a.], Brustbilder, Gruppenbildnis

Signatur des Originals: S 36/G03841

Briefwechsel zwischen Anastasius Grün [pseud.] und Ludwig August Frankl (1845-1876) /

Mode of access: Internet.

Briefwechsel zwischen Anastasius Grün

Mode of access: Internet.

DNA Mutation of the progranulin (GRN) gene in familial frontotemporal lobar degeneration (FTLD):a study of the pathology of nine cases

Frontotemporal lobar degeneration (FTLD) with transactive response (TAR) DNA-binding protein of 43kDa (TDP-43) proteinopathy (FTLD-TDP) is a neurodegenerative disease characterized by variable neocortical and allocortical atrophy principally affecting the frontal and temporal lobes. Histologically, there is neuronal loss, microvacuolation in the superficial cortical laminae, and a reactive astrocytosis. A variety of TDP-43 immunoreactive changes are present in FTLD-TDP including neuronal cytoplasmic inclusions (NCI), neuronal intranuclear inclusions (NII), dystrophic neurites (DN) and, oligodendroglial inclusions (GI). Many cases of familial FTLD-TDP are caused by DNA mutations of the progranulin (GRN) gene. Hence, the density, spatial patterns, and laminar distribution of the pathological changes were studied in nine cases of FLTD-TDP with GRN mutation. The densities of NCI and DN were greater in cases caused by GRN mutation compared with sporadic cases. In cortical regions, the commonest spatial pattern exhibited by the TDP-43 immunoreactive lesions was the presence of clusters of inclusions regularly distributed parallel to the pia mater. In approximately 50% of cortical gyri, the NCI exhibited a peak of density in the upper cortical laminae while the GI were commonly distributed across all laminae. The distribution of the NII and DN was variable, the most common pattern being a peak of NII density in the lower cortical laminae and DN in the upper cortical laminae. These results suggest in FTLD-TDP caused by GRN mutation: 1) there are greater densities of NCI and DN than in sporadic cases of the disease, 2) there is degeneration of the cortico-cortical and cortico-hippocampal pathways, and 3) cortical degeneration occurs across the cortical laminae, the various TDP-43 immunoreactive inclusions often being distributed in different cortical laminae.

A morphometric study of the spatial patterns of TDP-43 immunoreactive neuronal inclusions in frontotemporal lobar degeneration (FTLD) with progranulin (GRN) mutation

Mutations of the progranulin (GRN) gene are a major cause of familial frontotemporal lobar degeneration with transactive response (TAR) DNA-binding protein of 43 kDa (TDP-43) proteinopathy (FTLD-TDP). We studied the spatial patterns of TDP-43 immunoreactive neuronal cytoplasmic inclusions (NCI) and neuronal intranuclear inclusions (NII) in histological sections of the frontal and temporal lobe in eight cases of FTLD-TDP with GRN mutation using morphometric methods and spatial pattern analysis. In neocortical regions, the NCI were clustered and the clusters were regularly distributed parallel to the pia mater; 58% of regions analysed exhibiting this pattern. The NII were present in regularly distributed clusters in 35% of regions but also randomly distributed in many areas. In neocortical regions, the sizes of the regular clusters of NCI and NII were 400-800 µm, approximating to the size of the modular columns of the cortico-cortical projections, in 31% and 36% of regions respectively. The NCI and NII also exhibited regularly spaced clustering in sectors CA1/2 of the hippocampus and in the dentate gyrus. The clusters of NCI and NII were not spatially correlated. The data suggest degeneration of the cortico-cortical and cortico-hippocampal pathways in FTLD-TDP with GRN mutation, the NCI and NII affecting different clusters of neurons.

Wound healing and cancer progression in Opisthorchis viverrini associated cholangiocarcinoma

Letter to the editor