Guest Editors
Prosenjit Pal
University of Dundee; Yale School of Medicine
<p>Prosenjit Pal, PhD, is a biochemist specializing in organelle biology, proteomics, and neurodegenerative disease mechanisms. He earned his PhD in neuroscience from the S. N. Pradhan Centre for Neurosciences, University of Calcutta, India, and received the Newton-Bhabha PhD Fellowship in 2016-2017. His earlier research focused on the population genetics of Parkinson’s disease. Dr. Pal is currently a senior research associate and CRN Discovery Fellow, funded by ASAP, in the MRC Protein Phosphorylation and Ubiquitylation Unit at the University of Dundee, where he works with Prof. Dario Alessi.</p><p><br></p><p>Through this fellowship, he is also affiliated with Yale School of Medicine, collaborating with Prof. Shawn Ferguson. He is an active member of the Biochemical Society and the American Society for Biochemistry and Molecular Biology. His current research focuses on investigating the crosstalk between endolysosomal dysfunction and ciliogenesis in the context of Parkinson’s disease using mouse embryonic fibroblasts and human iPSC models.</p>
Shubhrajit Roy
Department of Physiology, Pharmacology, and Therapeutics, Johns Hopkins University
<p>Shubhrajit Roy, PhD, is a neuroscientist with expertise in metal homeostasis and brain physiology. He earned his doctoral degree in neuroscience from the S.N. Pradhan Centre for Neurosciences, University of Calcutta, India, and was awarded the Fulbright-Nehru Doctoral Research Fellowship (2018–2019). His research focuses on copper homeostasis in the choroid plexus, with particular emphasis on the mechanisms regulating copper entry into the brain and copper-mediated regulation of the cytoskeleton and cilia.</p><p><br></p><p>Currently, he is a postdoctoral fellow in the Department of Physiology, Pharmacology, and Therapeutics at Johns Hopkins University, where he works with Dr. Svetlana Lutsenko. He is an active member of the American Heart Association (AHA) and the Society for Neuroscience (SfN). His work integrates molecular, cellular, and in vivo approaches to understand how copper imbalance contributes to neurological disorders and to identify potential therapeutic strategies.</p>
Collection Overview
Neurodegenerative disorders are an increasingly urgent global health priority as they cause progressive deterioration of neuronal structure and function, leading to severe cognitive, motor, and behavioral impairment. Although conditions such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, Wilson’s disease, Menkes disease, and related disorders differ clinically, they often converge on shared cellular defects. Disrupted intracellular trafficking, altered organelle organization, impaired inter-organelle communication, and metabolic imbalance are central processes that weaken neuronal resilience and contribute to disease progression. Understanding these mechanisms is therefore essential for identifying common pathways of neurodegeneration and developing more effective therapeutic strategies.
This Topical Collection aims to provide the research community with a focused resource showcasing advanced experimental methods for investigating these interconnected cellular processes. The collection will highlight proteomics, live-cell imaging, synaptic vesicle recycling assays, endocytic flux measurements, and quantitative receptor trafficking approaches that enable detailed analysis of vesicular transport and endosomal recycling in neurons.
It will also emphasize methods for studying organelle contact sites involving mitochondria, endoplasmic reticulum, and lysosomes, including split fluorescent reporters, proximity ligation assays, and correlative light and electron microscopy. These techniques will support high-resolution investigation of organelle dynamics and communication in healthy and diseased cellular contexts. In addition, spatial metabolomics, lipidomics, and transcriptomics will be featured to examine carbohydrate and lipid metabolism within defined cellular environments.
By bringing together these methodological frameworks, this collection will help researchers quantitatively examine spatial, functional, and molecular changes that drive neurodegeneration, promoting reproducibility, cross-disease comparison, and mechanistic discovery.