Mitochondrial complex I inhibition enhances astrocyte responsiveness to pro-inflammatory stimuli.

Inhibition of the mitochondrial oxidative phosphorylation (OXPHOS) system can lead to metabolic disorders and neurodegenerative diseases. In primary mitochondrial disorders, reactive astrocytes often accompany neuronal degeneration and may contribute to neurotoxic inflammatory cascades that elicit brain lesions. The influence of mitochondria to astrocyte reactivity as well as the underlying molecular mechanisms remain elusive.

Analysis of the senescence-associated cell surfaceome reveals potential senotherapeutic targets.

The accumulation of senescent cells is thought to play a crucial role in aging-associated physiological decline and the pathogenesis of various age-related pathologies. Targeting senescence-associated cell surface molecules through immunotherapy emerges as a promising avenue for the selective removal of these cells. Despite its potential, a thorough characterization of senescence-specific surface proteins remains to be achieved.

Author Correction: BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

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Basic, Translational, and Clinical Research on Dementia.

The global impact of dementia is an increasing area of concern and, according to the Alzheimer's Disease International (ADI) World Alzheimer Report 2021, up to 90% of dementia patients in low- and middle-income countries are not diagnosed [...