Markus Daμμe

TMEM55B promotes anterograde transport and distal axonal distribution of LAMP1-positive organelles

This study shows TMEM55B and TMEM55A regulate lysosome distribution in neurons by affecting motor protein transport, with TMEM55B specifically promoting anterograde transport of LAMP1-positive organelles.

ER-Lysosome Cholesterol Exchange Regulates Lysosomal Motility Through mTOR-Dependent LAMTOR1 Phosphorylation

The paper identifies that lysosomal cholesterol exchange regulates motility through mTOR-dependent LAMTOR1 phosphorylation, revealing a feedback mechanism affecting mTORC1 activity and lysosomal movement.

Neurodegeneration risk variants promote lysosomal TMEM106B fibrilaccumulation

The paper identifies TMEM106B fibril accumulation as a shared mechanism in neurodegeneration linked to genetic variants in TMEM106B and GRN.

Fine-mapping reveals four TMEM106B haplotypes associated with neurodegenerative risk and preserved cognition at extreme age

Cleavage site-directed antibodies reveal the prion protein in humans is shed by ADAM10 at Y226 and associates with misfolded protein deposits in neurodegenerative diseases

This study identifies ADAM10-mediated shedding of human PrP at Y226 and shows sPrP associates with misfolded protein aggregates in neurodegenerative diseases.

Enhanced legumain activity links progranulin deficiency to TDP-43 pathology in frontotemporal lobar degeneration

This study shows that reduced progranulin leads to increased legumain activity, which promotes TDP-43 pathology in FTLD, suggesting legumain as a therapeutic target.

An AluYb8 retrotransposon characterises a risk haplotype of TMEM106B associated in neurodegeneration

The paper identifies an AluYb8 retrotransposon in a TMEM106B risk haplotype associated with neurodegeneration, linking it to age-related dysregulation and population-specific disease risk.

Multi cell line analysis of lysosomal proteomes reveals unique features and novel lysosomal proteins

The paper analyzes lysosomal proteomes across six cell lines to identify cell-type specific differences and novel lysosomal proteins.

Ligands binding to the cellular prion protein induce its protective proteolytic release with therapeutic potential in neurodegenerative proteinopathies

The paper shows that ligands binding to PrPC induce its proteolytic release, which has neuroprotective effects, and identifies mechanisms and exceptions in this process.