Paul M. A. Antony

Parkinson's disease-related Miro1 mutation induces mitochondrial dysfunction and loss of dopaminergic neurons in vitro and in vivo

This study shows that a Miro1 mutation causes mitochondrial dysfunction and dopaminergic neuron loss in both cell models and mice, supporting its role in Parkinson's disease.

DJ-1 mediates regulation of metabolism and immune response in Parkinsons disease astrocytes and Glioblastoma cells

This study shows DJ-1 affects metabolism and immune response differently in Parkinson's disease and glioblastoma cells, with antioxidant treatment rescuing PD-related phenotypes.

Insulin resistance compromises midbrain organoid neural activity and metabolic efficiency predisposing to Parkinsons disease pathology

This study shows insulin resistance in midbrain organoids reduces metabolic efficiency and neural activity, contributing to Parkinson's disease pathology.

Age-induced midbrain-striatum assembloids model early phenotypes of Parkinsons disease

This paper introduces midbrain-striatum assembloids with inducible aging to model early Parkinson's disease phenotypes and nigrostriatal connectivity.

Synaptic decline precedes dopaminergic neuronal loss in human midbrain organoids harboring a triplication of the SNCA gene

This study uses patient-specific midbrain organoids with SNCA triplication to show synaptic decline precedes dopaminergic neuron loss in Parkinson's disease.

Mitochondria-mitochondria interaction networks show altered topological patterns in Parkinson's disease

The paper analyzes mitochondria-mitochondria interaction networks in Parkinson's disease and finds altered topological patterns that correlate with clinical scores and can distinguish patients from controls.

Gene-corrected Parkinson's disease neurons show the A30P alpha-synuclein point mutation leads to reduced neuronal branching and function

This study shows that the A30P alpha-synuclein mutation in Parkinson's disease neurons reduces branching and function, with mitochondrial dysfunction and susceptibility to Rotenone.

IPSC-derived midbrain astrocytes from Parkinson's disease patients carrying pathogenic SNCA mutations exhibit alpha-synuclein aggregation, mitochondrial fragmentation and excess calcium release

Parkinson’s disease phenotypes in patient specific brain organoids are improved by HP-β-CD treatment

This study shows that HP-β-CD treatment improves dopaminergic differentiation in PD patient-derived midbrain organoids by enhancing mitophagy.