Columbia University
Irving Medical Center
Neurological Institute
710 West 168th Street, 3rd floor
(212) 305-1818
TaubCONNECT Research Perspective:
February 2023
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Cell Type-Specific Changes Identified by Single-Cell Transcriptomics in Alzheimer's Disease
Brain Aging Among Racially and Ethnically Diverse Middle-Aged and Older Adults
First Place: Neuroproteasome Localization and Dysfunction Modulate Pathology in Alzheimer's Disease
Clearance of an Amyloid-Like Translational Repressor is Governed by 14-3-3 Proteins
Diet Moderates the Effect of Resting State Functional Connectivity on Cognitive Function
Retromer Deficiency in Tauopathy Models Enhances the Truncation and Toxicity of Tau
Progranulin Mutations in Clinical and Neuropathological Alzheimer's Disease
Wolframin is a Novel Regulator of Tau Pathology and Neurodegeneration
Homotypic Fibrillization of TMEM106B Across Diverse Neurodegenerative Diseases
Correlation of Plasma and Neuroimaging Biomarkers in Alzheimer's Disease
Tubulin Tyrosination Regulates Synaptic Function and is Disrupted in Alzheimer's Disease
The Penalty of Stress - Epichaperomes Negatively Reshaping the Brain in Neurodegenerative Disorders
The Neuronal Retromer can Regulate Both Neuronal and Microglial Phenotypes of Alzheimer's Disease
Deep Learning Improves Utility of Tau PET in the Study of Alzheimer's Disease
Age of Onset of Huntington's Disease in Carriers of Reduced Penetrance Alleles
Caspase-9: A Multimodal Therapeutic Target With Diverse Cellular Expression in Human Disease
Midlife Vascular Factors and Prevalence of Mild Cognitive Impairment in Late-Life in Mexico
The Association Between Sex and Risk of Alzheimer's Disease in Adults with Down Syndrome
Marked Mild Cognitive Deficits in Humanized Mouse Model of Alzheimer's-Type Tau Pathology
Rapid ATF4 Depletion Resets Synaptic Responsiveness after cLTP
Polygenic Risk Score for Alzheimer's Disease in Caribbean Hispanics
Recognition Memory and Divergent Cognitive Profiles in Prodromal Genetic Frontotemporal Dementia
The Microtubule Cytoskeleton at the Synapse & The Synaptic Life of Microtubules
Optimizing Subjective Cognitive Decline to Detect Early Cognitive Dysfunction
The AD Tau Core Spontaneously Self-Assembles and Recruits Full-Length Tau to Filaments
Olfactory Impairment is Related to Tau Pathology and Neuroinflammation in Alzheimer's Disease
Pathogenic Role of Delta 2 Tubulin in Bortezomib-Induced Peripheral Neuropathy
Francesca Bartolini, PhDMicroglia Reactivity Entails Microtubule Remodeling from Acentrosomal to Centrosomal Arrays
Microglia cells are a specialized cell type that acts as a “sentinel” in our brain and plays critical roles in neuroinflammatory and neurodegenerative disease. Activating signaling triggers a change in microglia morphology that reflects a highly activated state associated with phagocytosis and proinflammatory function. The intracellular mechanisms driving microglia transition from the homeostatic to a reactive state are however poorly understood. This is partially due to challenges in imaging purified microglia without perturbing their homeostatic or reactive state.
Graphical Abstract. Microglia cell transition between homeostatic and reactive states is characterized by a dramatic reorganization of the microtubule cytoskeleton from a Golgi outpost-nucleated acentrosomal array to a pericentrosomal radial array to enable proper cytokine release.
In this manuscript, through in vitro phenotyping and in vivo validation, the Bartolini laboratory, together with collaborators from “Sapienza” University and the Institute of Technology in Italy, reports the break-through discovery that reactive microglia undergo a dramatic reorganization of their microtubule cytoskeleton, the most abundant cytoskeleton in the brain. As recently published in Cell Reports, we found that reactive microglia engage a unique example of microtubule transition from an array of parallel microtubules nucleated at Golgi-outposts to a radial array in which all the microtubules are anchored to a pericentrosomal region. Our findings suggest that this reorganization is critical for supporting the microglia “patrolling” and proinflammatory function, providing a novel target for reducing microglia reactivity in inflammatory and neurodegenerative disease. Given the role for spinal microglia in the remission and recurrence of neuropathic pain, this study may also pave the way to determine the contribution of microglial microtubule dysfunction in the etiology of neuropathic pain caused by chemotherapeutic drugs, most of which target the microtubule cytoskeleton.
These spearheading observations will set the ground to visualize microtubule remodeling as a dynamic marker of microglia activation, and to examine the impact of microtubule targeting drugs on microglia reactivity in neurodegenerative disease and microglia-mediated regulation of synaptic function.
Francesca Bartolini, PhD
Associate Professor of Pathology and Cell Biology at CUIMC
fb2131@cumc.columbia.edu
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