Optimizing the Translational Value of Mouse Models of ALS for Dysphagia Therapeutic Discovery.
Kate L Osman, Sabrina Kohlberg, Alexis Mok and 10 others
PMID 31300881WHAT IT FOUND
A low-copy ALS mouse model showed slower swallowing and tongue atrophy, while the common high-copy model showed slower swallowing without the same tongue atrophy.
Key findings
01Both SOD1 mouse models showed slower lick and swallow rates and longer intervals between swallows than controls, with the high-copy model more affected.
02Only the low-copy SOD1 mice showed significantly reduced tongue weight, surface area, total length, and caudal tongue length; the high-copy mice showed a trend that did not reach significance.
03Low-copy SOD1 mice had significantly fewer hypoglossal motor neurons than controls at advanced disease stage, with a loss within the range reported for high-copy SOD1 mice.
STILL TO COME
How it was doneWhat they foundWhat it means for SLPs
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What it does not show
The study used mice, not humans, so it cannot show what will happen in patients. The mouse airway anatomy meant no aspiration was seen, so absence of aspiration does not translate directly to human ALS swallowing safety. Swallowing was tested only at an advanced disease endpoint, not across early disease or progression. Some postmortem tissue was damaged or lost, reducing the number available for tongue and neuron analysis. Limb phenotype comparisons were preliminary and used a small descriptive classification. No treatment was tested, so the paper cannot guide a clinical intervention.
Declared interests
The authors declared no conflict of interest.
The easy way to misread this
Do not read this as evidence that a dysphagia therapy works for people with ALS. It tested mouse models only and did not evaluate treatment. The mice also showed no laryngeal penetration or aspiration, which does not translate directly to human ALS swallowing safety.