3,203 research outputs found
Age-related intracellular deposits of beta-amyloid and ubiquitin in the brain of healthy rats.
No full textThe malformation of the cerebellar fissura prima: a tool for studying histogenetic processes.
No full text
Axonal abnormalities in cerebellar Purkinje cells of the Ts65Dn mouse
No full textTs65Dn mice are a genetic model for Down syndrome. Among others, these mice have cerebellar pathology features which parallel those seen in Down syndrome patients. Both individuals with Down syndrome and Ts65Dn mice have reduced cerebellar volume and numbers of granule and Purkinje cells. In this report, we describe morphological abnormalities of axons of Purkinje cells in the cerebellum of Ts65Dn mice, by using anticalbindin immunocytochemistry. A consistent number of Purkinje cells shows axons bearing giant varicosities along their transit through the granular layer. The cerebellar arbor vitae made by fasciculated Purkinje cell axons has a patchy appearance, some tracks being devoid of calbindin staining. The infraganglionic plexus, formed by recurrent collaterals of Purkinje cell axons, has enormously increased density, which is evidence for a compensatory reaction to degeneration of distal segments of axons. These alterations are accompanied by strong glial reaction as evidenced by GFAP immunocytochemistry. Moreover, the alterations are more consistent in the anterior lobules of the vermis and intermediate cortex. The axonal pathology of Purkinje cells may explain the impairment in cerebellar functions observed in Ts65Dn mice at the adulthood
Purkinje cell damage in the cerebellum of immature rats following a single episode of early-life seizures.
No full textBeta-amyloid overload does not directly correlate with SAPK/JNK activation and tau protein phosphorylation in the cerebellar cortex of Ts65Dn mice.
No full textIt is known that in the nervous tissue β-amyloid overproduction and its extracellular or intracellular deposition can activate mitogen-activated protein kinases involved in tau protein phosphorylation. Hyperphosphorylated tau is not more able to bind neuron microtubules, leading to their disassembly and axon degeneration. We have previously described that at 10 months of age in the cerebellum of Ts65Dn mice, which are partially trisomic for the chromosome 16 and are considered a valuable model for Down syndrome, Purkinje cells undergo axon degeneration. Taking into consideration that Ts65Dnmice carry three copies of the gene encoding for theamyloid precursor protein, to characterize potential signaling events triggering the degenerative phenomenon, specific antibodies were used to examine the role of β-amyloid overload in the activation of the stress activated kinase/c-jun N-terminal kinase (SAPK/JNK) and tau protein phosphorylation in the cerebellar cortex of 12-month-old Ts65Dn mice. We found small extracellular deposits of β-amyloid at the borderline between the granule cell layer and the white matter, i.e., in the vicinity of the area where calbindin immunostaining of Purkinje cell axons revealed clusters of newly formed terminals of injured axons. Moreover, intracellular deposits were present in the somata of Purkinje cells. The level of activation of SAPK/JNK was greatly increased. The activation occurred in the “pinceaux” made by basket interneuron axons at the axon hillock of Purkinje cells. Antibody directed against tau protein phosphorylated at Ser-396/Ser-404 revealed positive NG2 cells and Bergman fibers in the molecular layer and oligodendrocytes in the white matter. Data indicate that β-amyloid extracellular deposits could have exerted a local cytotoxic effect, leading to Purkinje cell axon degeneration. The activation of SAPK/JNK in basket cell “pinceaux” may be a consequence of altered functionality of Purkinje cells and may represent an attempt of basket cells of synaptic remodeling. Moreover, the findings for tau protein phosphorylation suggest that Ts65Dnmice are affected by a cerebellar glial tauopathy
Glial cell reaction to cis-dichlorodiammineplatinum treatment in the immature rat cerebellum
No full textProteasome activity inhibition in cerebellar dysfuncion in a murine model of Down Syndrome.
No full textPurkinje cell axonal injury in the cerebellum of Ts65Dn mice: role of beta-amyloid overload
No full text
- …
