A TBK1 variant causes autophagolysosomal and motoneuron pathology without neuroinflammation in mice.

Although these findings could not be analyzed in vivo (due to limited signal quality from the respective antibodies in the mouse spinal cord tissue), a highly significant accumulation of galectin 8 + punctae was observed in human TBK1 E696K/E696K mutant iPSC-derived motor neurons that largely overlapped with LAMP1 ( Fig. 5, Q, T, and U ).

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A smaller group of female mice from surplus animal breeding was tested at the age of 18 mo only and revealed an inverted grid test deficit of TBK1 E696K/E696K knock-in mice that did not reach statistical significance ( Fig.

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The LC3-II/I ratio showed a trend toward a difference between both genotypes under untreated conditions, but it did not reach statistical significance ( Fig. 4 L ).

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