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Fig. 8 | Acta Neuropathologica Communications

Fig. 8

From: Elevated TMEM106B levels exaggerate lipofuscin accumulation and lysosomal dysfunction in aged mice with progranulin deficiency

Fig. 8

A model for the cross-regulation between TMEM106B and PGRN in the transgenic mouse model and in FTLD/PGRN patients with TMEM106B risk allele. Lysosomal dysfunction caused by PGRN deficiency during aging leads to TMEM106B accumulation, which results in more severe lysosomal pathology and eventually neuronal death in FTLD. PGRN might also play a direct role in regulating TMEM106B levels (dashed line)

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Acta Neuropathologica Communications

ISSN: 2051-5960

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