Researchers observed substantial physical improvements in the brain structures of the tested subjects.
"We found there was less brain atrophy and less tau accumulation, which was very exciting to see," said Huijie Huang.
In contrast, when scientists examined mice genetically altered to lack the Sorl1 gene responsible for producing SORLA, cellular damage and neurodegeneration accelerated significantly.
"The opposite turned out to be true when we deleted the ability to produce SORLA proteins," said Tim Huang, senior and corresponding author of the manuscript.
The absence of the protective protein intensified overall cognitive and structural degradation.
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"A lack of SORLA exacerbated the harmful effects observed in tauopathies," said Tim Huang.
Advanced cellular sequencing further showed that a lack of SORLA triggered the overactivation of specific receptor pathways in glial cells, which maintain the neuronal environment.
"One particularly notable finding that we can build on is the upregulation of a member of the plexin-B family of receptors in the absence of SORLA," said Huijie Huang.
This discovery highlights potential targets for existing pharmaceutical compounds.
"There are unique drugs that can target this class of receptors that we may be able to apply to tau-related dementia disorders," said Tim Huang.
Modulating these biological pathways could eventually offer remedies for cellular inflammation.
"One potential future direction is to repurpose these drugs to target overactivation of glial cells and perhaps reverse some of the phenotypes in tauopathies," said Tim Huang.
