Université de Fribourg

Microcalcification after excitotoxicity is enhanced in transgenic mice expressing parvalbumin in all neurones, may commence in neuronal mitochondria and undergoes structural modifications over time

Maetzler, W. ; Stünitz, H. ; Bendfeldt, Kerstin ; Vollenweider, F. ; Schwaller, Beat ; Nitsch, C.

In: Neuropathology and Applied Neurobiology, 2009, vol. 35, no. 2, p. 165 - 177

Aims: Parenchymal microcalcification in the brain coincides with neurodegenerative diseases, but is also frequently found in neurologically normal individuals. The origin and role of this process are still under debate. Parvalbumin (PV) is a protein acting as a Ca2+ buffer and Ca2+ shuttle towards intracellular Ca2+ sinks, like mitochondria and the endoplasmic reticulum. Constitutively, it is...

Université de Fribourg

The role of parvalbumin and calbindin D28k in experimental scrapie

Voigtländer, T. ; Unterberger, U. ; Guentchev, M. ; Schwaller, Beat ; Celio, Marco R. ; Meyer, M. ; Budka, H.

In: Neuropathology and Applied Neurobiology, 2008, vol. 34, no. 4, p. 435 - 445

Aims: Prion diseases are generally characterized by pronounced neuronal loss. In particular, a subpopulation of inhibitory neurones, characterized by the expression of the calcium-binding protein parvalbumin (PV), is selectively destroyed early in the course of human and experimental prion diseases. By contrast, nerve cells expressing calbindin D28k (CB), another calcium-binding protein, as well...