An inducedpluripotent stem cell (iPSC)-based model of KCNQ2-associated developmental epileptic encephalopathy suggests that disease is driven by dyshomeostaic neuronal mechanisms that are downstream of loss of M-current.

A mouse model of maturity-onset diabetes of the young illuminates that overactive TALK-1 channels limit β-cell calcium influx through membrane potential hyperpolarization, which blunts insulin secretion and causes glucose intolerance.

Drosophila ZIP13 (Slc39a13), a presumed zinc importer, is responsible for iron delivery to the secretory pathway.

Genetic sequencing has led to the increased diagnoses of rare diseases, strategies such as repurposing drugs and global metabolomics offer promise and bring hope to afflicted families.

Identification and characterization of multiple brain clusterin isoforms, including a mitochondrial matrix-targeted isoform, provides foundation to potentially clarify the link between these proteins and the development of late-onset Alzheimer’s disease.

In neurodegeneration of Gaucher disease, glucosylceramides trigger neuroinflammation via attrition of homeostatic microglia and transition to lipid-laden damage-associated microglia concurrently with infiltration of diverse immune cells including activated NK cells and CCR2⁺ macrophages, ameliorated by substrate reduction therapy.

In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

As worms age reduced glutathione together with increased ferrous iron increases frailty and leads to ferroptosis, which is amenable to therapeutic intervention.

A critical review of the limitations posed by current preclinical animal models of Alzheimer's disease and of the oversimplistic assumptions proposed by the amyloid cascade hypothesis (ACH).

A decline in iron-recycling functions of the splenic red pulp macrophages early during aging is driven by iron loading and involves their damage and a loss in red blood cell clearance capacity.