Philip C. Wong

The paper shows that restoring multiple TDP-43 cryptic targets, not just Unc13a, rescues motor neuron disease in a mouse model of ALS.

This study shows that preventing cryptic splicing of UNC13A and other TDP-43 targets can preserve memory and reduce neuron loss in a TDP-43 knockout mouse model.

BCG therapy reduces tau pathology and improves cognitive function in PS19 mice by modulating myeloid cell activity and neuroinflammation.

This study shows that TDP-43 dysfunction accelerates tauopathy, which primes co-filament assembly and dysfunction of TDP-43, exacerbating neuron loss in AD-LATE.

This study identifies brain region-specific TDP-43 pathology patterns in ageing, Alzheimer's disease, and amyotrophic lateral sclerosis, showing strong correlations with ferritin levels as a potential biomarker.

The paper identifies splicing dysregulation in Parkinson's disease linked to TDP-43 loss of function and shows its association with genetic mutations and cellular models.

This study uses a BBB-permeable AAV to deliver CTR and restore TDP-43 function in a mouse model of FTLD-TDP, reducing deficits and neuron loss.

AAV-PHP.eB-CTR gene therapy slows ALS progression and prevents paralysis in symptomatic mice by restoring TDP-43 function.

This study shows that senescent bone marrow adipocytes secrete SAP/PTX2, which promotes skeletal amyloidosis and bone loss in aging mice.

The paper identifies novel cryptic exons in TDP-43 deficient neurons by inhibiting nonsense-mediated decay, revealing potential therapeutic targets for ALS-FTD.

This paper shows that TDP-43 loss-of-function worsens tauopathy in a mouse model by increasing caspase 3-mediated tau cleavage in vulnerable neurons, leading to greater brain atrophy.

This study shows that elevated nuclear TDP-43 causes species-specific exon skipping, which differs from exon skipping seen in TDP-43 loss-of-function, highlighting the need for careful interpretation of TDP-43 overexpression models.

The paper uses large-scale RNA-seq data to show that ciclopirox triggers TDP-43 cryptic exon inclusion through oxidative stress and heavy metal toxicity.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

The paper identifies a fluid biomarker, cryptic HDGFL2, that detects early TDP-43 splicing repression in pre-symptomatic ALS patients.

This study shows that TDP-43 loss affects oligodendrocyte survival and myelination differently at various stages of maturation, leading to morphological defects and neurological impairments.

The paper identifies stage-specific microglia subtypes in Alzheimer's disease using single-cell RNA-sequencing, showing both amyloid-beta and tau pathologies are required for their induction.