Fredric P. Manfredsson

This study shows that dual inhibition of MLK3 and LRRK2 with URMC-099 reduces PD pathology and motor deficits in an AAV-haSyn rat model.

The paper investigates the role of MHCII reduction in protecting mice from alpha-synuclein-induced degeneration and finds that it is insufficient, while showing epigenetic regulation of the Parkinson's HLA locus.

This study identifies dopamine's role in devaluing reward memories through experimental and computational methods, showing its necessity for mediated devaluation and hedonic evaluation reduction.

This paper shows that combined Alzheimer's and Parkinson's protein pathologies enhance neuroinflammation and neurodegeneration in a mouse model.

This study investigates the role of CD8+ T cells in a mouse model of multiple system atrophy and finds they are not critical for disease progression but modulate neuroinflammation and demyelination.

This study examines changes in GDNF receptor expression in the striatum and substantia nigra following a nigrostriatal lesion in rats, finding differential expression patterns of GFR-1 and RET that may impact GDNF therapeutic efficacy.

This study shows nicotine promotes GABAergic neurons to adopt a dopaminergic phenotype, reducing alpha-synuclein-induced motor deficits in Parkinson's models.

The paper investigates how increased ser31 tyrosine hydroxylase phosphorylation in the substantia nigra compensates for dopamine loss and delays hypokinesia onset in a rat model of Parkinson's disease.

This study shows that IFNγ from CD4+ T cells drives neuroinflammation and demyelination in a mouse model of MSA.

This study shows that overexpressing Nurr1 in the striatum of rats induces LID and worsens dyskinesia, suggesting Nurr1 as a therapeutic target for Parkinson’s disease.

This study shows that oxytocin receptors in the dorsal raphe regulate serotonin-induced cortical plasticity, affecting prosocial behaviors in mother rats.

This study shows that α-synuclein aggregates cause c-Abl activation via redox stress, leading to neurodegeneration, and that N-acetyl cysteine can block this process in Parkinson's disease models.

The paper identifies DOPEGAL as a factor that promotes Tau pathology and propagation in locus coeruleus neurons via AEP cleavage of Tau.