Publications

Long-Term Safety and Clinical Effects of Nilotinib in Parkinson’s Disease

Nilotinib Effects on Safety, Tolerability, and Biomarkers in Alzheimer’s Disease

Towards a biomarker system that supports disease modifying therapies in Parkinson’s disease

Nilotinib Effects on Safety, Tolerability, and Potential Biomarkers in Parkinson Disease

Multikinase Abl/DDR/Src Inhibition Produces Optimal Efects for Tyrosine Kinase Inhibition in Neurodegeneration

Pharmacokinetics and pharmacodynamics of a single dose Nilotinib in individuals with Parkinson's disease

Tau clearance improves astrocytic function and brain glutamate-glutamine cycle.

Nilotinib Effects in Parkinson’s Disease and Dementia with Lewy Bodies

Inhibition of DDR1-BCR signalling by nilotinib as a new therapeutic strategy for metastatic colorectal cancer

Activating Autophagy as a Therapeutic Strategy for Parkinson's Disease.

Discoidin domain receptor inhibition reduces neuropathology and attenuates inflammation in neurodegeneration models.

Could cancer drugs be repurposed for use in Parkinson’s and Alzheimer’s?

Tyrosine kinase inhibition reverses TDP-43 effects on synaptic protein expression, astrocytic function and amino acid dis-homeostasis.

Two sides of the same coin: tyrosine kinase inhibition in cancer and neurodegeneration

Nilotinib and bosutinib modulate pre-plaque alterations of blood immune markers and neuro-inflammation in Alzheimer's disease models.

Tau deletion impairs intracellular β-amyloid-42 clearance and leads to more extracellular plaque deposition in gene transfer models

Tyrosine Kinase Inhibition Regulates Early Systemic Immune Changes and Modulates the Neuroimmune Response in αSynucleinopathy

Parkin-mediated reduction of nuclear and soluble TDP-43 reverses behavioral decline in symptomatic mice

Nilotinib-induced autophagic changes increase endogenous parkin level and ubiquitination, leading to amyloid clearance

Ubiquitination Increases Parkin Activity to Promote Autophagic a-Synuclein Clearance

Tyrosine kinase inhibition facilitates autophagic SNCA/α-synuclein clearance

Tyrosine kinase inhibition increases functional parkin‐Beclin‐1 interaction and enhances amyloid clearance and cognitive performance

Nilotinib reverses loss of dopamine neurons and improvesmotor behavior via autophagic degradation of a-synuclein in Parkinson’s disease models

Decreased parkin solubility is associated with impairment of autophagy in the nigrostriatum of sporadic Parkinson’s disease