Neurodegenerative diseases are characterized by the deposition of specific protein aggregates, both intracellularly and/or extracellularly, depending on the type of disease. The extracellular occurrence of tridimensional structures formed by amyloidogenic proteins defines Alzheimer's disease, in which plaques are composed of amyloid β-protein, while in prionoses, the same term "amyloid" refers to the amyloid prion protein. In this review, we focused on providing a detailed didactic description and differentiation of diffuse, neuritic, and burnt-out plaques found in Alzheimer's disease and kuru-like, florid, multicentric, and neuritic plaques in human transmissible spongiform encephalopathies, followed by a systematic classification of the morphological similarities and differences between the extracellular amyloid deposits in these disorders. Both conditions are accompanied by the extracellular deposits that share certain signs, including neuritic degeneration, suggesting a particular role for amyloid protein toxicity.

• Klíčová slova
• Alzheimer’s disease, Creutzfeldt–Jakob disease, Gerstmann–Sträussler–Scheinker syndrome, PrP plaques, amyloid, plaque subtypes, senile plaques,
• MeSH
• Alzheimerova nemoc metabolismus   MeSH
• amyloid metabolismus   MeSH
• amyloidní beta-protein metabolismus   MeSH
• amyloidní plaky metabolismus   MeSH
• amyloidogenní proteiny metabolismus   MeSH
• amyloidóza metabolismus   MeSH
• Creutzfeldtova-Jakobova nemoc metabolismus   MeSH
• lidé MeSH
• mozek metabolismus   patologie   MeSH
• neurity metabolismus   patologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• amyloid MeSH
• amyloidní beta-protein MeSH
• amyloidogenní proteiny MeSH

Schwann cell grafts support axonal growth following spinal cord injury, but a boundary forms between the implanted cells and host astrocytes. Axons are reluctant to exit the graft tissue in large part due to the surrounding inhibitory environment containing chondroitin sulphate proteoglycans (CSPGs). We use a lentiviral chondroitinase ABC, capable of being secreted from mammalian cells (mChABC), to examine the repercussions of CSPG digestion upon Schwann cell behaviour in vitro. We show that mChABC transduced Schwann cells robustly secrete substantial quantities of the enzyme causing large-scale CSPG digestion, facilitating the migration and adhesion of Schwann cells on inhibitory aggrecan and astrocytic substrates. Importantly, we show that secretion of the engineered enzyme can aid the intermingling of cells at the Schwann cell-astrocyte boundary, enabling growth of neurites over the putative graft/host interface. These data were echoed in vivo. This study demonstrates the profound effect of the enzyme on cellular motility, growth and migration. This provides a cellular mechanism for mChABC induced functional and behavioural recovery shown in in vivo studies. Importantly, we provide in vitro evidence that mChABC gene therapy is equally or more effective at producing these effects as a one-time application of commercially available ChABC.

• MeSH
• astrocyty metabolismus   MeSH
• axony metabolismus   MeSH
• buněčná adheze MeSH
• centrální nervový systém metabolismus   MeSH
• chondroitinasa ABC metabolismus   MeSH
• chondroitinsulfát proteoglykany metabolismus   MeSH
• genetická terapie MeSH
• integriny metabolismus   MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• Lentivirus enzymologie   MeSH
• neurity metabolismus   MeSH
• neuroglie metabolismus   MeSH
• neurony metabolismus   MeSH
• periferní nervový systém metabolismus   MeSH
• pohyb buněk MeSH
• poranění míchy patofyziologie   MeSH
• potkani Sprague-Dawley MeSH
• regenerace nervu účinky léků   MeSH
• Schwannovy buňky metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• chondroitinasa ABC MeSH
• chondroitinsulfát proteoglykany MeSH
• integriny MeSH

Brain development is determined by neuronal differentiation including changes of cell polarity and asymetric growth of neuronal processes. Although, there are many unkown factors contributing to changes of lenght of neuronal cones, mounting experimental and review papers focus on changes of growth conus and role of axonal transport. In particular, mechanisms of actin/microtubule polymerisation and depolymerisation are important. Role of intracellular calcium is also significant. Normal and properly timed changes of lenght of axons and dendrites are dependent on interaction of neurons and glia. Moreover, regeneration of injured axons is dependent on growth factors secreted from glial cells. The aim of the present study is characterisation of the most important mechanisms underlying changes of lenght of neurites.

• MeSH
• aktiny metabolismus   MeSH
• axony metabolismus   fyziologie   MeSH
• buňky - růstové procesy fyziologie   MeSH
• dendrity metabolismus   fyziologie   MeSH
• lidé MeSH
• mikrotubuly metabolismus   MeSH
• neurity metabolismus   fyziologie   MeSH
• neurony cytologie   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• aktiny MeSH