Acta Neuropathologica: Direct nerve transfer of vCJD/BSE after the monkey finger is cut open.

Non-human primates appear to be the closest model for studying human medically-sourced prion diseases.
here, we report the consequences of the mutant KYA/Mad Cow Disease (vCJD/BSE) vaccination on the fingers of crab-eating monkeys, demonstrating the actual risks of primitive transmission patterns and occupational exposure.
in the brain, PrPd deposits are layered deep in the cortical, deposited heavily in the hyalural, substrate, cer cerebral and brain trunks.
distribution of PrPd in the spinal cord, mainly in the glial and Clarke back cores, while the level of PrPd was significantly reduced.
sediments throughout the central nervous system are diverse: synapses, nerve peripherals, mesh aggregates, small plaques, plaques, and incomplete plaques.
retinal clumps are marked with no amyloid or tau deposits.
the abnormal PrPd deposits are arranged along deuterks, short and long axles, axon-shaped fine meshes, or pearl strings.
they exist in the deep new cortical, substrate and motor neurons.
this lengthy process is not common, but has been reported in human and experimental studies.
: Cut the far sides of a 4-year-old macaque's right middle finger to induce local inflammation, and then inject the equivalent of 10 milligrams of BSE to attack the macaque's brain.
after 18 months of finger clumsiness, clinical disorders (behavioural abnormalities, fear, sensory allergies, gait disorders, tremors) began to appear 7.5 months after vaccination and euthanasia two months later.
speed of the right-hand positive nerve is reduced to 1/3 of the corresponding part on the left side, and the sensory cause is not detected.
to conduct histological and biochemical studies as described earlier.
All components of the triad are present: spongi-like changes in the neo-cortical, sprite, and brain trunks are moderate, changes in the spinal cord are mild, but changes in the hyaluralurological and neural brains are severe; neuron loss is generally moderate, but severe in the small brain and myelin (empty blister neurons);
ELISA and Western blot (WB) showed that PrPres had the expected BSE glycoprotein aggregation pattern at all levels of the brain and spinal cord.
, we have observed that primates exposed to vCJD/BSE through distant finger damage, after 7.5 years of silent incubation, can lead to large amounts of PrPd deposition, severely restricted to the nervous system and eyes.
Mkol, J., Delmotte, J., Jouy, D. et al. Direct neural transmission of vCJD/BSE in macaque after finger incision. Acta Neuropathol (2020). MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Original" are owned by Mets Medicine and are not authorized to be reproduced by any media, website or individual, and are authorized to be reproduced with the words "Source: Mets Medicine".
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