NR ANZY
AU Bons,N.
TI Spontaneous spongiform encephalopathy in a monkey - reply
QU Lancet 1996 Oct 5; 348(9032): 956
PT Letter
VT
SIR - Baker and colleagues' main criticism is that the clinical and pathological features shown by the Montpellier monkey Macaca mulatta differed from those of cynomolgus monkey (Macaca fascicularis) experimentally infected with BSE. These differences raise questions on the nature and origin of the neurodegenerative disorder noted in the Montpellier monkey, since the lesion profile seen in animals naturally or experimentally infected with BSE is uniform within each species. We agree with this point of view. However, in our report we did not suggest a link to BSE; we advanced the possibility of transmission of the disease through prion-contaminated foodstuff, similar to that proposed for BSE. Thus, the two models (spontaneous degeneration without known cause versus intracerebral inoculation with BSE) are not readily comparable, and clinicopathological differences are conceivable.
The Montpellier monkey was not examined clinically in detail, and few data have been obtained from animal attendants. Presumably, the monkey showed neurological signs in addition to behavioural changes, since the involvement of the brain the pathological process was extensive, as specified below. Nevertheless, abnormal behavioural signs similar to those shown by our monkey (eg, edginess) have been also noted in the initial stage of the experimental spongiform encephalopathy of BSE-infected macaques.
With respect to the neuropathological features of the Montpellier monkey, spongiform changes were prominent in many grey structures, including the cerebral cortex, striatum, thalamus, and cerebellar cortex. Changes in the white matter were minor, and were related to enlargement of nerve-cell processes without demyelination. The spongiform changes were associated with PrP and ß-protein deposition.
In view of Baker and colleagues' concerns, we will undertake other immunohistochemical investigations (no frozen tissue is available for immunoblot analysis) with a large panel of antibodies to PrP. However, the labelling reported in the monkey was not shown in the lemurian primate (Microcebus murinus) species investigated in my laboratory. With respect to the ß-amyloid plaques, the results were obtained with several monoclonal and polyclonal antibodies, and with thioflavin S and PAM silver impregnation in three different laboratories (Montpellier, Bons; Boston, Mesulam; Milan, Tagliavini) and these results cannot be contested.
Noelle Bons
Ecole Practique Des Hautes Etudes, Laoratoire De Neuromorphologie. Fonctionelle, 34095 Montpellier, France
ZR 0 Zitate
SP englisch
OR Prion-Krankheiten 2