In: Cellular and Molecular Life Sciences CMLS, 2005, vol. 62, no. 10, p. 1120-1130
|
In: Journal of Neurology, 2004, vol. 251, p. v57-v64
|
In: Brain, 2005, vol. 128, no. 1, p. 52-63
|
In: Brain, 2012, vol. 135, no. 7, p. 2169-2177
|
In: Toxicological Sciences, 2012, vol. 125, no. 1, p. 209-218
|
In: Brain, 2015, vol. 138, no. 2, p. 388-397
|
In: Brain, 2008, vol. 131, no. 1, p. 288-303
|
In: Brain, 2002, vol. 125, no. 1, p. 75-85
|
In: Brain, 2008, vol. 131, no. 10, p. 2679-2689
|
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...
|