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Johns Hopkins researchers have identified a specific cell death pathway that leads to the physical and intellectual degeneration related to Parkinson's.
It's imperative that Parkinson's patients go to hospital stays with a prepared attitude, an advocate, and medication info, says columnist Sherri Woodbridge.
Assistant Secretary for HUD's Office of Policy Development and Research (PD&R) Raphael Bostic and his executive staff provide an overview of what their offic...
Learn from Dr. Martin McKeown, MD, Director of Pacific Parkinson’s Research Centre, how Parkinson's disease (PD) symptoms and signs affect multiple systems o...
Article and image by Vince Giuliano Stem cell injections have been shown to improve symptoms of Parkinson’s Disease (PD) in a rat model, essentially providing a “cure” for the disease. This is after 20 years of research on stem cell therapies for PD. When then will a stem cell therapy be available for PD in
Merkel cell carcinoma (MCC) is a rare and aggressive skin cancer associated with advanced age and immunosuppression. Over the past decade, an association has been discovered between MCC and either integration of the Merkel cell polyomavirus, which likely drives tumorigenesis, or somatic mutations owing to ultraviolet-induced DNA damage. Both virus-positive and virus-negative MCCs are immunogenic, and inhibition of the programmed cell death protein 1 (PD-1)–programmed cell death 1 ligand 1 (PD-L1) immune checkpoint has proved to be highly effective in treating patients with metastatic MCC; however, not all patients have a durable response to immunotherapy. Despite these rapid advances in the understanding and management of patients with MCC, many basic, translational and clinical research questions remain unanswered. In March 2018, an International Workshop on Merkel Cell Carcinoma Research was held at the US National Cancer Institute, at which academic, government and industry experts met to identify the highest-priority research questions. Here, we review the biology and treatment of MCC and report the consensus-based recommendations agreed upon during the workshop. Merkel cell carcinoma (MCC) is a rare and aggressive form of nonmelanoma skin cancer. The availability of immune checkpoint inhibition has improved the outcomes of a subset of patients with MCC, although many unmet needs continue to exist. In this Consensus Statement, the authors summarize developments in our understanding of MCC while also providing consensus recommendations for future research.
Recently I attended a PD about flipped classrooms where students complete readings, lectures, and/or research prior to the start of class. In this age of technology, I loved this idea. However, I also worry about the digital divide so I thought I could include the flipped classroom format into my daily routine. During the pandemic,…
Parkinson’s disease (PD) is an age-related movement disorder caused by the loss of dopaminergic (DA) neurons of the substantia nigra pars compacta (SNpc) of the midbrain, however, the underlying cause(s) of this DA neuron loss in PD is unknown and there are currently no effective treatment options to prevent or slow neuronal loss or the progression of related symptoms. It has been shown that both environmental factors as well as genetic predispositions underpin PD development and recent research has revealed that lysosomal dysfunction and lipid accumulation are contributors to disease progression, where an age-related aggregation of alpha-synuclein as well as lipids have been found in PD patients. Interestingly, the most common genetic risk factor for PD is Glucosylceramidase Beta 1 (GBA), which encodes a lysosomal glucocerebrosidase (GCase) that cleaves the beta-glucosidic linkage of lipids known as glucocerebrosides (GluCer). We have recently discovered that artificial induction of GluCer accumulation leads to cellular senescence of DA neurons, suggesting that lipid aggregation plays a crucial role in the pathology of PD by driving senescence in these vulnerable DA neurons. Here, we discuss the relevance of the age-related aggregation of lipids as well as the direct functional link between general lipid aggregation, cellular senescence, and inflammaging of DA neurons. We propose that the expression of a cellular senescence phenotype in the most vulnerable neurons in PD can be triggered by lysosomal impairment and lipid aggregation. Importantly, we highlight additional data that perilipin (PLIN2) is significantly upregulated in senescent DA neurons, suggesting an overall enrichment of lipid droplets (LDs) in these cells. These findings align with our previous results in dopaminergic neurons in highlighting a central role for lipid accumulation in the senescence of DA neurons. Importantly, general lipid droplet aggregation and global lysosomal impairment have been implicated in many neurodegenerative diseases including PD. Taken together, our data suggest a connection between age-related lysosomal impairment, lipid accumulation, and cellular senescence in DA neurons that in turn drives inflammaging in the midbrain and ultimately leads to neurodegeneration and PD.
Kim Burgess | Chicago Pd | Marina Squerciati | Adam Ruzek | Patrick Flueger | Ramona Edith Williams | Makayla Burgess
“y'all are sick. harassing me when i'm already at my limits https://t.co/c1VjUikEQu”
Chicago PD - Kim Burgess