Publications by authors named "R M PITKIN"
This article explores what it means to work with decontextualized or mysterious archival traces within collections that already contain obscured provenance. In particular, it compels us to consider what a single object can tell us about the individual, Dr. Magnus Hirschfeld, and what it can teach us about the larger queer community from which it may have originated.
View Article and Find Full Text PDFParkinson's disease (PD) and dementia with Lewy bodies (DLB) are progressive neurodegenerative diseases for which there is no disease-modifying treatment. PD and DLB are characterized by aggregation of the synaptic protein α-synuclein, and there is compelling evidence to suggest that progression of these diseases is associated with the trans-cellular spread of pathogenic α-synuclein through the brains of afflicted individuals. Therapies targeting extracellular, pathogenic α-synuclein may therefore hold promise for slowing or halting disease progression.
View Article and Find Full Text PDFArticle Synopsis
- - The immune system plays a key role in sporadic Alzheimer's disease (sAD), with genetic risk factors highlighting its importance in the disorder's mechanisms.
- - Studies of microglia in human brains show that their activation is linked to the progression of Alzheimer's, particularly when beta-Amyloid and tau pathology are present together.
- - Variants in the TREM2 gene lead to altered microglial responses, which may affect treatment strategies for sAD due to significant differences in immune activation across brain regions and genetic backgrounds.
In Lewy body diseases-including Parkinson's disease, without or with dementia, dementia with Lewy bodies, and Alzheimer's disease with Lewy body co-pathology -α-synuclein (α-Syn) aggregates in neurons as Lewy bodies and Lewy neurites . By contrast, in multiple system atrophy α-Syn accumulates mainly in oligodendrocytes as glial cytoplasmic inclusions (GCIs) . Here we report that pathological α-Syn in GCIs and Lewy bodies (GCI-α-Syn and LB-α-Syn, respectively) is conformationally and biologically distinct.
View Article and Find Full Text PDFAims: The aim of this study was to test the hypothesis that different conformations of misfolded α-synuclein (α-syn) are present in Parkinson's disease (PD) brain.
Methods: Using two previously characterized conformations of α-syn fibrils, we generated new conformation-selective α-syn monoclonal antibodies (mAbs). We then interrogated multiple brain regions in a well-characterized autopsy cohort of PD patients (n = 49) with these mAbs, Syn7015 and Syn9029.