This neuronal pathway is referred to as the cerebellum to Purkinje cell climbing fiber pathway and it is implicated in the coordination of movements

Scientists in the Laboratoire de Neurobiologie des Processus Adaptatifs (CNRS/Université Pierre et Marie Curie) have shown that it is possible to repair an injured brain by creating a small number of new, specifically-targeted innervations, rather than a larger number of non-specific connections. Behavioral tests have demonstrated that such reinnervation can thus restore damaged cerebral functions.
Brain injury in adults can cause irreparable, long-term physical and cognitive damage. However, motor and spatial functions can be recovered if undamaged neurons are stimulated to create new innervation. This type of innervation develops spontaneously after a brain injury in very young children.
Researchers had previously shown – based on injury to the neuronal pathway linking the stem to the cerebellum(1) – it was possible to induce reinnervation in young adults similar to that observed in newborn infants. This repair was rendered possible by treating the damaged cerebellum with a peptide(2) called Brain Derived Neurotrophic Factor (BDNF) which plays a role in the development and satisfactory functioning of this neuronal pathway.
In the present case, the researchers have extended the use of this model and showed that the terminals of new axons interact with the network of undamaged neuronal cells to restore their associated functions, such as synchronized movement and spatial orientation. These results demonstrate a correlation between an improvement in behavior and the degree of reinnervation in the cerebellum. Thus a small amount of correctly-targeted reinnervation makes it possible to recover fine functions such as motor and cognitive skills.
These results open promising new perspectives and make it possible to envisage using BDNF – already employed during clinical trials on the treatment of neurodegenerative conditions such as Parkinson's disease – to repair the human brain after a cerebral lesion.
1) This neuronal pathway is referred to as the cerebellum to Purkinje cell climbing fiber pathway and it is implicated in the coordination of movements.
2) A protein that is normally present in the brain and is involved in its development and functioning.
Journal reference: Melina L. Willson, Catriona McElnea, Jean Mariani, Ann M. Lohof, and Rachel M. Sherrard. BDNF increases homotypic olivocerebellar reinnervation and associated fine motor and cognitive skill. Brain on April 1st, 2008.
Not sure where the origin of this text

Hope this is another step in the right direction Alan, and thanks once again for the information

Very True.

Another step forward is

the Wales Raredisease Implentation Plan

I am sure you are aware, I am involved with its production, public launch, its progress and its upcoming review and I am very keenand will make sure its outcomes are carried out.

Welsh Government launch plan to tackle rare diseases (Broadcast on National TV on Raredisease Day)


RareDisease "Warrior"

More fantastic work from the Welsh government. All the rare diseases put together must put a real strain on the NHS

I think you must be refering to the media spin.

They conveinently didnt say all the good stuff, like Wales advises ALL the worlds on medical issues, as it has most of the top centres, like the European Stem Cell Centre plus the Cancer Centre…


Thanks for the hard work Alan. Brilliant source of information. It was good news in the new addition of the ataxian about sca2, but the added information we receive from you is invaluable. To a true warrior

I am called the Raredisease “warrior” in many circles around the world !

Its on - when you would type in the names of the authors and some words

With a free fulltext readable for everybody!

Citations from the fulltext:

In conclusion, our findings support the hypothesis that BDNF alterations are involved in neurodegenerative mechanisms and suggest that low BDNF levels are nonspecific markers of neurodegeneration common to several cognitive disorders.


Are there already studies for the substitution of BDNF existing?

In my understanding it is not enough clarified which level/amount of BDNF would be helpful to try to attain/to hold.

Furthermore, some medications are influencing the level of BDNF you would have got, and also different diseases haven been described as connected with typical lower or higher levels of BDNF.

Kind regards,