Richard Wade‐Martins

The paper uses patient-derived iPSC-dopamine neurons to screen compounds and identifies the FASN-SREBP1 axis as a potential therapeutic target for Parkinson's disease.

This study shows simvastatin reduces PD-related phenotypes in iPSC-derived neurons by inhibiting RhoA, with RhoA activity varying across PD subtypes.

This paper creates a humanised GBA-L444P mouse model to study GBA1 mutations in Parkinson's, finding gain-of-function effects on dopamine release and loss-of-function effects on alpha-synuclein pathology.

The paper investigates dopamine release defects in Parkinson's patient-derived neurons and identifies reduced VMAT2 function as the cause.

This study shows that SARM1 activation causes mitochondrial dysfunction in human neurons, which can be reversed by nicotinamide or prevented by antisense oligonucleotides.

The paper examines TFEB and TFE3 expression and function in brain cells, showing TFEB is restricted to glia while TFE3 is widespread, with distinct roles in mitochondrial and lysosomal biogenesis in neurons.

This study shows USP30 inhibition improves mitochondrial health through both PINK1-dependent and independent mechanisms, enhancing mitophagy and mitochondrial efficiency in neurons.

The paper identifies Anxa1+ dopamine neurons as vulnerable in prodromal Parkinson's disease, linking their dysfunction to bradykinesia and procedural motor learning impairments.

This study investigates how C-terminal truncations of alpha-synuclein (aSyn) affect Lewy body (LB) formation and pathology in Parkinson's disease by analyzing their role in fibril processing and aggregation.

This study shows that the GBA-N370S mutation causes early hyperexcitability in striatal neurons by reducing sodium and potassium currents, which can be mitigated by aging or PKA antagonism.

The paper profiles spatial transcriptomic and translatomic data of dopaminergic neurons in young and old mice, identifying markers of aging and disease-related pathways, and highlights CASR as a novel regulator of dopaminergic calcium handling.

This study shows that reducing tau in human neurons decreases A beta toxicity, supporting the role of tau in Alzheimer's disease mechanisms.

This study uses proteomic techniques to show that PGRN deficiency impairs lysosomal function and proteostasis in neurons by altering pH, enzyme levels, and protein turnover.

The paper uses PET imaging to show increased dopamine D2 receptor binding in LRRK2-R1441C rats, suggesting receptor upregulation as a compensatory response to dopamine deficits.

This study shows iPSC-derived astrocytes from AD patients reflect key pathophysiological features, offering a new model for AD research and therapeutic screening.

This study uses a novel proteomics platform to identify PTM dysregulation in GBA-N370S PD neurons, revealing impaired neuritogenesis and a role for tau.

The paper uses induced pluripotent stem cell-derived cortical neurons from early Alzheimer's patients to show that cellular vulnerability to amyloid-beta correlates with clinical vulnerability.

This study identifies altered mitochondrial and energy metabolism in PARK2 mutant human iPSC-derived dopaminergic neurons through metabolomic analysis.

This study shows that inhibiting SUV4-20 H1 increases frataxin expression in FRDA cells and patient-derived cells, suggesting it as a therapeutic target.

This study develops a transgenic mouse model expressing human alpha-synuclein in noradrenergic neurons, revealing LC pathology and non-motor PD features.

The paper constructs a single-cell atlas of the Substantia nigra and identifies cell-specific gene expression patterns linked to Parkinson's disease and neuropsychiatric disorders.

The DPUK Data Portal provides secure access to cohort data for dementia research, supporting multi-modal analyses and collaborations across multiple institutions.

The paper investigates the role of astrocytic GABA transporters in regulating dopamine release in the striatum and shows their downregulation in early parkinsonism.

Calpain-1/2 cleavage of the alpha-synuclein C-terminus after fibril formation is reported to drive seeding, aggregation and the maturation of Lewy-body-like inclusions in primary neurons.