Good news! Why not eliminate pain genes or sneeze genes etc.? Or convert pain associated genes into laugh genes? 😄
Remember the animals (mice) that suffered for this progress to be achieved (I blogged here, here about it)!
"A gene-silencing technique based on CRISPR can relieve pain in mice, according to a study. ... it is a promising approach for squelching chronic pain that lasts for months or years. ...
The new version of CRISPR doesn’t edit genes directly — it stops them from being expressed — and so shouldn’t cause permanent changes, although it’s unclear how long its effects last for. ...
Although there are many types of ion channel, studies have suggested that a sodium channel called Nav1.7 could play a central part in chronic pain. When people have mutations in the gene coding for this channel, they either experience extreme, constant pain, or can’t feel any pain at all. ...
[researchers] thought they might be able to stop pain signals travelling to the brain by preventing neurons from producing Nav1.7. Chemists have been trying to block Nav1.7 with small-molecule drugs and antibodies, but have struggled because these therapies also interact with structurally similar sodium channels in the body, causing side effects including numbness and poor coordination. ...
The pain relief seemed to last, in some cases, for as long as 44 weeks after the injection. ..."
The new version of CRISPR doesn’t edit genes directly — it stops them from being expressed — and so shouldn’t cause permanent changes, although it’s unclear how long its effects last for. ...
Although there are many types of ion channel, studies have suggested that a sodium channel called Nav1.7 could play a central part in chronic pain. When people have mutations in the gene coding for this channel, they either experience extreme, constant pain, or can’t feel any pain at all. ...
[researchers] thought they might be able to stop pain signals travelling to the brain by preventing neurons from producing Nav1.7. Chemists have been trying to block Nav1.7 with small-molecule drugs and antibodies, but have struggled because these therapies also interact with structurally similar sodium channels in the body, causing side effects including numbness and poor coordination. ...
The researchers attached to the modified Cas9 a second, ‘repressor’ protein that stops the Nav1.7 gene from being expressed. The researchers packaged this system in a small, inactive virus called an adeno-associated virus that could shuttle it into cells.
They gave mice a spinal injection of the gene-silencing therapy, then tried to induce chronic pain by injecting the animals with chemotherapy drugs or inflammatory agents. ...The pain relief seemed to last, in some cases, for as long as 44 weeks after the injection. ..."
"... In particular, a hereditary loss-of-function mutation in NaV1.7, a sodium channel protein associated with signaling in nociceptive sensory afferents, leads to insensitivity to pain without other neurodevelopmental alterations. However, the high sequence and structural similarity between NaV subtypes has frustrated efforts to develop selective inhibitors. ..."
Here is the link to the underlying research paper:
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