Diego E Rincon-Limas

Diego E Rincon-Limas, PhD

Associate Professor & University Term Professor

Department: MD-BEHAVIORAL NEUROLOGY
Business Phone: (352) 273-9689

About Diego E Rincon-Limas

Dr. Rincon-Limas received a bachelor degree on Biopharmaceutical Chemistry from the Autonomous University of Tamaulipas in Reynosa, Mexico. He also obtained a Master’s degree in Microbiology and a summa cum laude Ph.D. in Molecular Biology and Genetic Engineering at the Autonomous University of Nuevo Leon in Monterrey, Mexico. He then moved to Baylor College of Medicine in Houston to conduct his postdoctoral training in the Department of Human and Molecular Genetics, where he got training in Neurogenetics and Neurobiology. He got his first Faculty position in the Department of Neurology and the Mitchell Center for Neurodegenerative Disorders at the University of Texas Medical Branch in Galveston, and then moved to the University of Florida to join the Department of Neurology at the McKnight Brain Institute. He has a joint appointment in the Department of Neuroscience and is also a member of the UF Genetics Institute, the Center for Translational Research in Neurodegenerative Disease (CTRND), and the Center for Neurogenetics.

Accomplishments

Exemplary Teacher Award
2020 · University of Florida College of Medicine
Exemplary Teacher Award
2018 · University of Florida College of Medicine
Exemplary Teacher Award
2017 · University of Florida College of Medicine
University Term Professorship Award
2017 · University of Florida

Teaching Profile

Courses Taught
2019-2024
GMS6757 Introduction to Alzheimer’s Disease and Related Dementias: Clinical and Mechanistic Principles
2017-2024
GMS6096 Introduction to NIH Grant Writing for Biomedical Sciences
2019
ENY6905 Problems in Entomology
2018
GMS7980 Research for Doctoral Dissertation
2017
BMS4905 Medical Sciences Senior Research
2014
GMS6223 Drosophila Neurogen
2013
GMS7794 Neuroscience Seminar

Research Profile

Neurodegenerative disorders, including Alzheimer’s disease, frontotemporal dementia, amyotrophic lateral sclerosis, Parkinson’s disease and prion diseases, are some of the most dreaded conditions in our society. These conditions affect millions of people worldwide, represent a huge and increasing burden on the health-care system, and constitute one of the major challenges of modern medicine. Unfortunately, the pathogenic mechanisms underlying these debilitating disorders are poorly understood and, therefore, there are no effective therapies to avoid their fatal outcome.

My laboratory focuses on the development and application of new technologies to define the molecular pathways leading to neurodegeneration and to identify potential therapeutic targets. To do so, we utilize the fruit fly Drosophila melanogaster to model molecular, biochemical and pathological aspects of human neurodegenerative conditions. This is achieved by disrupting homologous genes in Drosophila, or by expressing a human disease gene in this organism. Strikingly, the remarkable genetic conservation from flies to humans leads to neurological phenotypes that closely mimic the human disease. Once the model is validated, we apply a multidisciplinary approach combining Drosophila genetics, neurobiology, molecular biology, biochemistry, optogenetics and systems biology. My goal is to use this multidisciplinary effort to dissect unknown, fundamental events that mediate these devastating pathologies.

Open Researcher and Contributor ID (ORCID)

0000-0003-3099-0642

Publications

2023
Amyloid fibril proteomics of AD brains reveals modifiers of aggregation and toxicity.
Molecular neurodegeneration. 18(1) [DOI] 10.1186/s13024-023-00654-z. [PMID] 37710351.
2023
Identification of potential pathways and biomarkers linked to progression in ALS
Annals of Clinical and Translational Neurology. 10(2):150-165 [DOI] 10.1002/acn3.51697. [PMID] 36533811.
2023
Insights from Drosophila on Aβ- and tau-induced mitochondrial dysfunction: mechanisms and tools.
Frontiers in neuroscience. 17 [DOI] 10.3389/fnins.2023.1184080. [PMID] 37139514.
2022
Infection and chronic disease activate a brain-muscle signaling axis that regulates muscle performance.
bioRxiv : the preprint server for biology. [DOI] 10.1101/2020.12.20.423533. [PMID] 33398283.
2022
Nuclear import receptors are recruited by FG-nucleoporins to rescue hallmarks of TDP-43 proteinopathy.
Molecular neurodegeneration. 17(1) [DOI] 10.1186/s13024-022-00585-1. [PMID] 36482422.
2022
TDP-35, a truncated fragment of TDP-43, induces dose-dependent toxicity and apoptosis in flies.
Neural regeneration research. 17(11):2441-2442 [DOI] 10.4103/1673-5374.338997. [PMID] 35535891.
2021
Molecular, functional, and pathological aspects of TDP-43 fragmentation
iScience. 24(5) [DOI] 10.1016/j.isci.2021.102459. [PMID] 34013172.
2021
Starvation and activity dependent modulation of salt taste behavior in Drosophila.
Alzheimer's & dementia (Amsterdam, Netherlands). 17(Suppl 12) [DOI] 10.1002/alz.058538. [PMID] 35845712.
2021
TDP-43 and ER Stress in Neurodegeneration: Friends or Foes?
Frontiers in molecular neuroscience. 14 [DOI] 10.3389/fnmol.2021.772226. [PMID] 34759799.
2020
Aß40 displays amyloidogenic properties in the non-transgenic mouse brain but does not exacerbate Aß42 toxicity in Drosophila.
Alzheimer's research & therapy. 12(1) [DOI] 10.1186/s13195-020-00698-z. [PMID] 33069251.
2020
NCBP2 modulates neurodevelopmental defects of the 3q29 deletion in Drosophila and Xenopus laevis models
PLOS Genetics. 16(2) [DOI] 10.1371/journal.pgen.1008590. [PMID] 32053595.
2020
PhotoGal4: A Versatile Light-Dependent Switch for Spatiotemporal Control of Gene Expression in Drosophila Explants.
iScience. 23(7) [DOI] 10.1016/j.isci.2020.101308. [PMID] 32652492.
2018
Bringing Light to Transcription: The Optogenetics Repertoire.
Frontiers in genetics. 9 [DOI] 10.3389/fgene.2018.00518. [PMID] 30450113.
2018
Engineered Hsp70 chaperones prevent Aβ42-induced memory impairments in a Drosophila model of Alzheimer’s disease.
Scientific reports. 8(1) [DOI] 10.1038/s41598-018-28341-w. [PMID] 29967544.
2018
Lmx1a is required for the development of the ovarian stem cell niche in Drosophila.
Development (Cambridge, England). 145(8) [DOI] 10.1242/dev.163394. [PMID] 29615466.
2018
Short Aβ peptides attenuate Aβ42 toxicity in vivo
Journal of Experimental Medicine. 215(1):283-301 [DOI] 10.1084/jem.20170600. [PMID] 29208777.
2017
A KCNC3 mutation causes a neurodevelopmental, non-progressive SCA13 subtype associated with dominant negative effects and aberrant EGFR trafficking.
PloS one. 12(5) [DOI] 10.1371/journal.pone.0173565. [PMID] 28467418.
2017
Anti-Aβ single-chain variable fragment antibodies restore memory acquisition in a Drosophila model of Alzheimer’s disease.
Scientific reports. 7(1) [DOI] 10.1038/s41598-017-11594-2. [PMID] 28900185.
2017
Drosophila models of prionopathies: insight into prion protein function, transmission, and neurotoxicity.
Current opinion in genetics & development. 44:141-148 [DOI] 10.1016/j.gde.2017.03.013. [PMID] 28415023.
2017
secHsp70 as a tool to approach amyloid-β42 and other extracellular amyloids
Fly. 11(3):179-184 [DOI] 10.1080/19336934.2017.1291104. [PMID] 28165856.
2016
A single amino acid (Asp159) from the dog prion protein suppresses the toxicity of the mouse prion protein in Drosophila.
Neurobiology of disease. 95:204-9 [DOI] 10.1016/j.nbd.2016.07.025. [PMID] 27477054.
2016
Data set of interactomes and metabolic pathways of proteins differentially expressed in brains with Alzheimer׳s disease.
Data in brief. 7:1707-19 [DOI] 10.1016/j.dib.2016.04.071. [PMID] 27257613.
2016
Holdase activity of secreted Hsp70 masks amyloid-β42 neurotoxicity in Drosophila.
Proceedings of the National Academy of Sciences of the United States of America. 113(35):E5212-21 [DOI] 10.1073/pnas.1608045113. [PMID] 27531960.
2016
Identification of proteins that are differentially expressed in brains with Alzheimer’s disease using iTRAQ labeling and tandem mass spectrometry.
Journal of proteomics. 139:103-21 [DOI] 10.1016/j.jprot.2016.03.022. [PMID] 27012543.
2015
Anti-Aβ single-chain variable fragment antibodies exert synergistic neuroprotective activities in Drosophila models of Alzheimer’s disease.
Human molecular genetics. 24(21):6093-105 [DOI] 10.1093/hmg/ddv321. [PMID] 26253732.
2015
Modeling the complex pathology of Alzheimer’s disease in Drosophila.
Experimental neurology. 274(Pt A):58-71 [DOI] 10.1016/j.expneurol.2015.05.013. [PMID] 26024860.
2014
Combined pharmacological induction of Hsp70 suppresses prion protein neurotoxicity in Drosophila.
PloS one. 9(2) [DOI] 10.1371/journal.pone.0088522. [PMID] 24523910.
2014
KCNC3(R420H), a K(+) channel mutation causative in spinocerebellar ataxia 13 displays aberrant intracellular trafficking.
Neurobiology of disease. 71:270-9 [DOI] 10.1016/j.nbd.2014.08.020. [PMID] 25152487.
2014
Launching Hsp70 neuroprotection: two drugs better than one.
Cell cycle (Georgetown, Tex.). 13(11):1657-8 [DOI] 10.4161/cc.29148. [PMID] 24810400.
2014
Mutations in Helix 3 Promote Cross-Seeding of Prp-Wt and Neurotoxicity
Prion. 8(S)
2013
Polar substitutions in helix 3 of the prion protein produce transmembrane isoforms that disturb vesicle trafficking.
Human molecular genetics. 22(21):4253-66 [DOI] 10.1093/hmg/ddt276. [PMID] 23771030.
2013
Purification of transcripts and metabolites from Drosophila heads.
Journal of visualized experiments : JoVE. (73) [DOI] 10.3791/50245. [PMID] 23524378.
2013
p∆TubHA4C, a new versatile vector for constitutive expression in Drosophila.
Molecular biology reports. 40(9):5407-15 [DOI] 10.1007/s11033-013-2639-7. [PMID] 23681549.
2012
Differential activation of the ER stress factor XBP1 by oligomeric assemblies.
Neurochemical research. 37(8):1707-17 [DOI] 10.1007/s11064-012-0780-7. [PMID] 22528838.
2012
Drosophila models of proteinopathies: the little fly that could.
Current pharmaceutical design. 18(8):1108-22 [PMID] 22288402.
2012
Identifying Protective Prp Residues With Flies-Insights Into the Dog Prp-N158D Substitution
Prion. 6
2011
Amyloid-beta42 interacts mainly with insoluble prion protein in the Alzheimer brain.
The Journal of biological chemistry. 286(17):15095-105 [DOI] 10.1074/jbc.M110.199356. [PMID] 21393248.
2011
Pulling rabbits to reveal the secrets of the prion protein.
Communicative & integrative biology. 4(3):262-6 [DOI] 10.4161/cib.4.3.15054. [PMID] 21980555.
2011
The ER stress factor XBP1s prevents amyloid-beta neurotoxicity.
Human molecular genetics. 20(11):2144-60 [DOI] 10.1093/hmg/ddr100. [PMID] 21389082.
2010
Exploring prion protein biology in flies: genetics and beyond.
Prion. 4(1):1-8 [PMID] 20083902.
2010
Sequence-dependent prion protein misfolding and neurotoxicity.
The Journal of biological chemistry. 285(47):36897-908 [DOI] 10.1074/jbc.M110.174391. [PMID] 20817727.
2009
In vivo generation of neurotoxic prion protein: role for hsp70 in accumulation of misfolded isoforms.
PLoS genetics. 5(6) [DOI] 10.1371/journal.pgen.1000507. [PMID] 19503596.
1998
Lhx2, a vertebrate homologue of apterous, regulates vertebrate limb outgrowth.
Development (Cambridge, England). 125(20):3925-34 [PMID] 9735354.
1993
Association between genetic variation at the porphobilinogen deaminase gene and schizophrenia.
Schizophrenia research. 8(3):211-21 [PMID] 8094629.
1990
Three polymorphisms at the D17S29 locus.
Nucleic acids research. 18(16) [PMID] 1975670.
1990
Two MspI RFLPs at the D17S258 locus.
Nucleic acids research. 18(23) [PMID] 1702207.

Grants

Dec 2022 ACTIVE
Harnessing new targets and mechanisms mediating AD pathogenesis
Role: Principal Investigator
Funding: NATL INST OF HLTH NIA
Dec 2022 ACTIVE
Nuclear import receptors as modifiers of TDP-43 phase transition and toxicity in FTD/ALS
Role: Principal Investigator
Funding: MAYO CLINIC via NATL INST OF HLTH NIA
Aug 2020 – May 2023
Functional assessment of 1,500 human genes against coexistent Abeta and tau pathology in vivo
Role: Principal Investigator
Funding: NATL INST OF HLTH NIA
Aug 2018 ACTIVE
Deconstructing and challenging TDP-43 proteinopathies: from FTLD/ALS to Alzheimers disease
Role: Principal Investigator
Funding: NATL INST OF HLTH NIA
Jun 2018 – Feb 2021
Exploring the unparalleled protection of RAF2 against Abeta42 and tau toxicity
Role: Principal Investigator
Funding: NATL INST OF HLTH NIA
Sep 2017 – Jun 2020
Uncovering targets that block pathological interactions between Abeta and tau
Role: Principal Investigator
Funding: NATL INST OF HLTH NIA
Feb 2017 – Sep 2019
Large-scale identification of genes that suppress concurrent Abeta42 and tau pathology in vivo
Role: Principal Investigator
Funding: FL DEPT OF HLTH ED ETHEL MOORE ALZHEIMER
Apr 2016 – Mar 2019
Targeting nuclear transport dysfunction in TDP-43 proteinopathies
Role: Principal Investigator
Funding: NATL INST OF HLTH NINDS
Nov 2015 ACTIVE
Optogenetic systems to regulate light-mediated transcription with spatiotemporal resolution
Role: Principal Investigator
Funding: LIFE SCIENCES RESEARCH FOUNDATION via HUGHES MEDICAL INST, HOWARD
Jul 2014 – Jun 2017
Optogenetic modeling of primary and secondary CNS proteinopathies in Drosophila
Role: Principal Investigator
Funding: NATL INST OF HLTH NINDS
Jul 2013 – Dec 2015
Engineering chaperones for extracellular amyloids
Role: Principal Investigator
Funding: NATL INST OF HLTH

Contact Details

Phones:
Business:
(352) 273-9689
Emails:
Addresses:
Business Mailing:
PO Box 100236
GAINESVILLE FL 32610
Business Street:
1149 NEWELL DR RM L3 100
GAINESVILLE FL 32610