Drosophila ClC-c Is a Homolog of Human CLC-5 and a New Model for Dent Disease Type 1.

Key Points: can be a model for Dent Disease type 1. Clc-C mutations function similar to human CLC-5 Dent 1 mutations.

Background: serve as exceptional alternative models for and research and may provide an avenue for in-depth investigation for human ClC-5 and Dent disease type 1 (DD1).

Protein retention in the endoplasmic reticulum rescues Aβ toxicity in Drosophila.

Amyloid β (Aβ) accumulation is a hallmark of Alzheimer's disease. In adult Drosophila brains, human Aβ overexpression harms climbing and lifespan. It's uncertain whether Aβ is intrinsically toxic or activates downstream neurodegeneration pathways.