What is your doctor going to do with this information to help your recovery? You probably need to train your doctor in this.
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A team of researchers led by professor Patrik Verstreken (VIB/KU
Leuven) has exposed the fine details of a mechanism that provides more
insight in the communication between neurons. The research has clarified
how damaged synapses – the connection points between neurons – are
repaired to keep communication between neurons at an optimal level.
Disturbances in these mechanisms are believed to play a role in the
development of neurodegenerative diseases, such as dementia, ALS or
Parkinson’s disease. The results have been published in leading
neuroscience journal ‘Neuron’.
Our brains are made up of billions
and billions of nerve cells or neurons that gather and transmit signals
via so-called synapses. These synaptic connections between neurons
transmit ‘electrical firings’ via chemical messengers
(neurotransmitters). Synapses thus contribute to numerous bodily
functions, including speech, thoughts and voluntary actions.
Disruption of synaptic transmission
Prof.
Patrik Verstreken (VIB/KU Leuven): “Synapses are the active part of
neurons, and this activity causes some damage in the long term.
Fortunately, synapses are capable of breaking down and ‘recycle’ damaged
cellular components. Our study has largely revealed the process behind
this. It is quite a significant discovery, especially when you consider
that many neurological diseases, such as Parkinson’s, ALS or dementia,
but also speech or motion disorders for instance, are caused by the
disruption of synaptic transmission.”
Cellular debris
Prior
research revealed that several different proteins play a role in
neuronal communication. However, these same proteins can also cause
disruptions. This happens, for instance, when proteins split, causing
their particles to stick together and clump. This ‘cellular debris’ then
disrupts synaptic transmissions and may contribute to the development
of neurodegenerative diseases.
The importance of ‘microautophagy’
Prof.
Patrik Verstreken (VIB/KU Leuven): “We studied the proteins involved,
both in vitro and in vivo and, in doing so, exposed a mechanism called
‘synaptic microautophagy’. This mechanism helps ‘clean up’ cellular
debris at the synapse, by engulfing the debris in a membrane and then
removing it, for instance. It ensures that the cellular debris is
isolated from the rest of the synapse. We found that synaptic
communication slows down when microautophagic activity is reduced (i.e.
when the cellular debris is not broken down) and that it speeds up when
microautophagic activity increases (when more cellular debris is broken
down). This discovery therefore represents an important advance in the
search for treatments for neurodegenerative diseases, such as
Alzheimer’s – which are caused by clumped together cellular debris.”
Pathways for further research
The
study conducted by prof. Verstreken and his team once again emphasizes
the need for ongoing research into neuronal communication. Such research
could examine substances that may counteract the progress of
neurodegeneration in neurons. This would aid the search for potential
drug treatments for neurological diseases, such as Alzheimer’s.
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