Our doctors with just a little bit of more research help should be able to figure out how to solve memory problems in stroke survivors. But of course our fucking failures of stroke associations will not followup this research to make it translational. You're continuously screwed.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=163796&CultureCode=en
Universität Bonn
Researchers from Germany and the USA have identified an important
mechanism with which memory switches from recall to memorization mode.
The study may shed new light on the cellular causes of dementia. The
work was directed by the University of Bonn and the German Center for
Neurodegenerative Diseases (DZNE). It is being published in the renowned
journal “Neuron.”
Because of its shape, the control center of memory bears the poetic
name of “hippocampus” (seahorse). New sensations to be stored
continually enter this region of the brain. But at the same time, the
hippocampus is also the guardian of memories: It retrieves stored
information from the depths of memory.
The hippocampus is also an important transport junction. And just
like rush hour in a major city, it also needs a regulating hand to
control the opposing flows of information. The researchers from Bonn,
Los Angeles and Palo Alto have now identified such a memory traffic
policeman. Certain cells in the brain, the hippocampal astrocytes,
ensure that the new information is given priority. The mind thus
switches into memorization mode; by contrast, the already saved memories
must wait.
However, the astrocytes themselves only take orders: They react to
the neurotransmitter acetylcholine, which is released in particular in
novel situations. It has been known for several years that acetylcholine
promotes the storage of new information. How this happens has only been
partly understood. “In our work, we were able to show for the first
time that acetylcholine stimulates astrocytes which then are induced to
release the transmitter glutamate,” explains Milan Pabst, who is a
doctoral candidate at the Laboratory for Experimental Epileptology of
the University of Bonn. “The released glutamate then activates
inhibitory nerve cells which inhibit a pathways mediating the retrieval
of memories.”
The researchers working with the neuroscientist Prof. Dr. Heinz Beck
genetically modified nerve cells so that they could be activated by
light and then release acetylcholine. Using this trick, they were able
to clarify the mechanism using recordings in living brain tissue
sections. “However, we also show that, in the brains of living mice,
acetylcholine has the same effect on the activity of the neurons,”
explains Pabst’s colleague, Dr. Holger Dannenberg.
Astrocytes have long since been underestimated
Another reason this result is interesting is because astrocytes
themselves are not nerve cells. They belong to what are known as glial
cells. Until the turn of the millennium, they were still considered to
merely serve as mechanical support to the real stars of the brain, the
neurons.
In recent decades, however, it has become increasingly clearer that
this image is far from correct. It is known by now that astrocytes can
release neurotransmitters – the messengers by which neurons communicate
with each other – or even remove them from the brain. “It was previously
unknown that the astrocytes are involved in central memory processes
through the mechanism which has now been discovered,” explains Prof.
Beck. However, an observation made by US scientists in 2014 fits into
this context: If astrocytes’ function is inhibited, this has a negative
effect on the recognition of objects.
The results may also shed new light on the cellular causes of memory
disorders. Thus there are indications that the controlled secretion of
acetylcholine is disrupted in patients with Alzheimer’s dementia.
“However, we have not investigated whether the mechanism we discovered
is also impacted,” stresses Pabst.
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