For a better experience, click the Compatibility Mode icon above to turn off Compatibility Mode, which is only for viewing older websites.

Peter Baas

Peter Baas, PhD

Professor; Director, Graduate Program in Neuroscience


Department: Neurobiology & Anatomy

Education

  • Postdoctoral Fellowship - Temple University
  • PhD - Michigan State University

Awards & Honors

  • Drexel Provost Award for Outstanding Scholarly Productivity – Career (2019)

Peter Baas, PhD, is a professor in the Department of Neurobiology & Anatomy at Drexel University College of Medicine. He is also director of the graduate program in neuroscience.

Research Overview

Baas laboratory research image, microtubule arrays of the neuron.

The Baas Laboratory focuses on the underlying mechanisms of neurodegeneration and dysfunction of the nervous system, resulting from degenerative diseases, developmental disorders and injury, with the goal of developing therapies for prevention, treatment and repair. Rather than focusing on just one type of disease, disorder or injury, we focus on a common downstream target that goes awry across almost all of them. By focusing downstream, we can gain mechanistic insights and develop therapies that can broadly apply across maladies. This enables each lab member to have a distinctive project while keeping everyone on a unified mission. Specifically, the downstream target we study is the microtubule – a cytoskeletal structure that is critically important for all aspects of the architecture, intracellular transport and mobility of neurons and other cells of the nervous system.

Lab Members

Research Assistant Professor and Lab Co-director: Dr. Liang Qiang

Senior Scientist and Lab Manager: Dr. Wenqian Yu

Senior Postdoctoral Fellow:  Dr. Emanuela Piermarini

Graduate Students: Ankita Patil, Hemalatha Muralidharan, Philip Yates, Shrobona Guha and Xiaohuan Sun

Research Interests

Degeneration, dysfunction, injury and repair of the nervous system

Research

Project 1. Neurodevelopmental Disorders

As neurons develop from mitotic precursors, they undergo a migratory journey to their final locations in the brain or elsewhere in the body. Axons develop with growth cones heralding their journey to their targets, and dendrites form as well. Both axons and dendrites undergo extensive branching, pruning and remodeling. All of these events are microtubule-based, with the relevant proteins and pathways vulnerable to disorders such as autism. For over 30 years, we have worked to elucidate the mechanisms, proteins and pathways of neurodevelopment to enable us to have unique insights into such neurodevelopmental disorders that we are now studying.

Project 2. Hereditary Spastic Paraplegia

Hereditary spastic paraplegia (HSP) is (usually) an adult-onset disease that most often arises due to autosomal dominant mutations of the SPAST gene, which encodes for a microtubule-severing protein called spastin. The patients have a pronounced gait deficiency and eventually become confined to a wheelchair, due to corticospinal degeneration. Our focus on microtubules has provided us unique insights into the etiology of the disease, which we are studying with various experimental models. In the past we have used cultured rodent neurons and Drosophila, but now we are using a mouse model for HSP that we have developed that displays the hallmark characteristics of the disease. We are conducting behavioral, anatomical and histochemical studies, pursuing molecular mechanisms, and are now poised to begin testing therapies. We also have developed human-induced pluripotent cell lines (hiPSC) from patients with the disease, which we are differentiating into neurons, for further analyses of mechanisms and potential therapies.

Watch a lecture from Dr. Baas for patients and their caregivers

Project 3. Disease of Tau

Tau is a microtubule-associated protein that goes awry in Alzheimer’s disease, coming off the microtubules to form neurofibrillary tangles. Many other diseases also involve abnormalities to tau including frontotemporal dementia, supranuclear palsy, and Parkinson’s disease, as well as injuries such as traumatic brain injury. Most researchers in the field believe that microtubules become destabilized in tau diseases, but our hypothesis is different – we posit that tau is important for keeping much of the microtubule content of the axon labile and dynamic and that tau diseases cause the loss of the labile/dynamic component of the microtubule array. We also posit that microtubules become disorganized in the axon as a result of toxic properties of the abnormal tau. We are using mouse models and hiPSC lines from human patients to test our hypotheses and pursue novel therapies.

Read about our work in Science Daily

Project 4. Gulf War Illness

A substantial portion of the veterans who served in the 1991 Gulf War suffer from a disease called Gulf War illness (GWI). The symptoms are mainly of the CNS (central nervous system), including memory deficits, sleep disorders, headache and fatigue. Our lab is part of the Gulf War Illness Consortium, a group of researchers and physicians from around the country who work collaboratively to understand the etiology of this mysterious disease and develop therapies. The disease seems to have arisen from a combination of stress of the battlefield together with various toxicants such as the neurotoxin sarin as well as pesticides. We are using rodent models and hiPSC lines (that we developed) in 2-dimensional culture and 3-dimensional cerebral organoids to test our hypothesis that microtubule abnormalities underlie the neurodegeneration and develop novel therapies accordingly.

Read about our work in the College of Medicine Alumni Magazine and Science Daily

Project 5. Spinal Cord Injury

Our laboratory is part of the Marion Murray Spinal Cord Research Center, which is a multidisciplinary group of labs at Drexel University aimed at developing novel approaches for improving the lives of people suffering from spinal cord injuries (SCI). Mostly in collaboration with our partner labs, we are striving to use our knowledge of microtubule-based pathways to prompt injured nerves in the spinal cord to regenerate in ways that lead to functional recovery.

Mentoring

“Unbeknownst to her, neuroscience student Hemalatha Muralidharan was listening to her future mentor when she heard Peter Baas, PhD, speak at a conference she attended as an undergraduate in Mumbai, India. The topic, and his way of talking about it, piqued her interest. Years later, when Hema came to the College of Medicine to pursue her PhD in the Graduate School of Biomedical Sciences and Professional Studies, she visited the Baas Lab and found both a home for her research and a mentor who inspired her.”

Read more

Drexel neuroscience student Hemalatha Muralidharan with Drexel faculty, Peter Baas, PhD

In the Media

Publications

Selected Publications

"Tau: It's Not What You Think"
Baas PW, Qiang L
Trends Cell Biol. 2019 Mar 28. pii: S0962-8924(19)30038-8. doi: 10.1016/j.tcb.2019.02.007. [Epub ahead of print] Review. PMID: 30929793

"Mitotic Motor KIFC1 is an organizer of microtubules in the axon"
Muralidharan H, Baas PW
J Neurosci. 2019 Feb 25. pii: 3099-18. doi: 10.1523/JNEUROSCI.3099-18.2019. [Epub ahead of print] PMID: 30804089

"Knockdown of Fidgetin Improves Regeneration of Injured Axons by a Microtubule-Based Mechanism"
Matamoros AJ, Tom VJ, Wu D, Rao Y, Sharp DJ, Baas PW
J Neurosci. 2019 Mar 13;39(11):2011-2024. doi: 10.1523/JNEUROSCI.1888-18.2018. Epub 2019 Jan 15. PMID: 30647150

"Hereditary spastic paraplegia: gain-of-function mechanisms revealed by new transgenic mouse"
Qiang L, Piermarini E, Muralidharan H, Yu W, Leo L, Hennessy LE, Fernandes S, Connors T, Yates PL, Swift M, Zholudeva LV, Lane MA, Morfini G, Alexander GM, Heiman-Patterson TD, Baas PW
Hum Mol Genet. 2019 Apr 1;28(7):1136-1152. doi: 10.1093/hmg/ddy419. PMID: 30520996

"Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9-mediated kif15 mutations accelerate axonal outgrowth during neuronal development and regeneration in zebrafish"
Dong Z, Wu S, Zhu C, Wang X, Li Y, Chen X, Liu D, Qiang L, Baas PW, Liu M
Traffic. 2019 Jan;20(1):71-81. doi: 10.1111/tra.12621. Epub 2018 Nov 29. PMID: 30411440

"Tau Does Not Stabilize Axonal Microtubules but Rather Enables Them to Have Long Labile Domains"
Qiang L, Sun X, Austin TO, Muralidharan H, Jean DC, Liu M, Yu W, Baas PW
Curr Biol. 2018 Jul 9;28(13):2181-2189.e4. doi: 10.1016/j.cub.2018.05.045. Epub 2018 Jun 28. PMID: 30008334

"Polarity Sorting of Microtubules in the Axon"
Rao AN, Baas PW
Trends Neurosci. 2018 Feb;41(2):77-88. doi: 10.1016/j.tins.2017.11.002. Epub 2017 Nov 30. Review. PMID: 29198454

"Polarity sorting of axonal microtubules: a computational study" [PDF]
Craig EM, Yeung HT, Rao AN, and Baas PW
Molecular Biology of the Cell 28(23):3271-3285. doi:10.1091/mbc.E17-06-0380 (November 2017)

"Nanoparticle Delivery of Fidgetin siRNA as a Microtubule-based Therapy to Augment Nerve Regeneration" [PDF]
Austin TO, Matamoros AJ, Friedman JM, Friedman AJ, Nacharaju P, Yu W, Sharp DJ & Baas PW
Scientific Reports, 7:9675, DOI:10.1038/s41598-017-10250-z (August 2017)

"Cytoplasmic Dynein Transports Axonal Microtubules in a Polarity-Sorting Manner" [PDF]
Rao AN, Patil A, Black MM, Craig EM, Myers KA, Yeung HT & Baas PW
Cell Reports, 19, 2210–2219 (June 2017)

"Pharmacologically increasing microtubule acetylation corrects stress-exacerbated effects of organophosphates on neurons"
Rao AN, Patil A, Brodnik ZD, Qiang L, España RA, Sullivan KA, Black MM, Baas PW
Traffic, 18(7):433-441. doi: 10.1111/tra.12489. Epub 2017 May 25 (July 2017)

"Reprogramming cells from Gulf War veterans into neurons to study Gulf War illness"
Qiang L, Rao AN, Mostoslavsky G, James MF, Comfort N, Sullivan K, Baas PW
Neurology, 88(20):1968-1975. doi: 10.1212/WNL.0000000000003938 (May 16, 2017)

"Truncating mutations of SPAST associated with hereditary spastic paraplegia indicate greater accumulation and toxicity of the M1 isoform of spastin" [PDF]
Solowska JM, Rao AN, and Baas PW
Molecular Biology of the Cell 28(13):1728-1737. doi:10.1091/mbc.E17-01-0047 (May 2017)

"Mutant spastin proteins promote deficits in axonal transport through an isoform-specific mechanism involving casein kinase 2 activation" [PDF]
Lanfranco Leo, Carina Weissmann, Matthew Burns, Minsu Kang, Yuyu Song, Liang Qiang, Scott T. Brady, Peter W. Baas, and Gerardo Morfini
Human Molecular Genetics, doi: 10.1093/hmg/ddx125 (epub April 7, 2017)

"Microtubules in Health and Degenerative Disease of the Nervous System" [PDF]
Matamoros AJ, Baas PW
Brain Res Bull. 126(Pt 3):217-225. doi: 10.1016/j.brainresbull.2016.06.016. Epub 2016 Jun 27. (September 2016)

"Stability Properties of Neuronal Microtubules" [PDF]
Baas PW, Rao AN, Matamoros AJ, Leo L
Cytoskeleton, 73:442–460 (September 2016)

"Microtubules: Organization and Function in Neurons Introductory Article"
P.W. Baas, K.A. Myers, L. Qiang, V.C. Nadar
In: Reference Module in Biomedical Sciences, pub: Elsevier B.V. (2014)

"Mitotic motors coregulate microtubule patterns in axons and dendrites"
Lin S, Liu M, Mozgova OI, Yu W, Baas PW
J Neurosci. 32(40):14033-49 (Oct 3, 2012).

"Septin-driven coordination of actin and microtubule remodeling regulates the collateral branching of axons"
Hu J, Bai X, Bowen JR, Dolat L, Korobova F, Yu W, Baas PW, Svitkina T, Gallo G, Spiliotis ET.
Curr Biol. 22(12):1109-15 (Jun 19, 2012).

M"icrotubule redistribution in growth cones elicited by focal inactivation of kinesin-5"
Nadar VC, Lin S, Baas PW
J Neurosci. 32(17):5783-94 (Apr 25, 2012).

"Partial interruption of axonal transport due to microtubule breakage accounts for the formation of periodic varicosities after traumatic axonal injury"
Tang-Schomer MD, Johnson VE, Baas PW, Stewart W, Smith DH
Exp Neurol. 233(1):364-72 (Jan 2012).

"Hooks and Comets: The Story of Microtubule Polarity Orientation in the Neuron"
Baas PW, Lin S
Developmental Neurobiology; 71(6):403-418 (June 21, 2011).

"Kinesin-5, a mitotic microtubule-associated motor protein, modulates neuronal migration"
Falnikar A, Tole S, and Baas PW
Molecular Biology of the Cell; 22:1561-1574 (May 1, 2011).

"Inhibition of kinesin-5, a microtubule-based motor protein, as a strategy for enhancing regeneration of adult axons"
Lin S, Liu M, Son YJ, Himes BT, Snow DM, Yu W, Baas PW
Traffic; 12:269-286 (Jan 17, 2011).

"Strategies for diminishing katanin-based loss of microtubules in tauopathic neurodegenerative diseases"
Sudo H, Baas PW
Human Molecular Genetics; 20(4):763-778 (Feb 15, 2011).

"Kinesin-12, a mitotic microtubule-associated motor protein, impacts axonal growth, navigation, and branching"
Liu M, Nadar VC, Kozielski F, Kozlowska M, Yu W, Baas PW
Journal of Neuroscience; 30(44):14896-906 (Nov 3, 2010).

"Evaluation of loss of function as an explanation for SPG4-based hereditary spastic paraplegia"
Solowska JM, Garbern JY, Baas PW
Human Molecular Genetics;19(14):2767-2779 (Jul 15, 2010).

"Acetylation of microtubules influences their sensitivity to severing by katanin in neurons and fibroblasts"
Sudo H and Baas PW
Journal of Neuroscience; 30(21):7215–7226 (May 26, 2010).

"Mechanical breaking of microtubules in axons during dynamic stretch injury underlies delayed elasticity, microtubule disassembly, and axon degeneration"
Tang-Schomer MD, Patel AR, Baas PW, and Smith DH
FASEB Journal; (5):1401-1410 (May 24 2010).

"Basic Fibroblast Growth Factor Elicits Formation of Interstitial Axonal Branches via Enhanced Severing of Microtubules"
Qiang L, Yu W, Liu M, Solowska JM, and Baas PW
Molecular Biology of the Cell; 21(2):334 –344 (Jan 15, 2010).

"Kinesin-5 is Essential for Growth-Cone Turning"
Nadar VC, Ketschek A, Myers KA, Gallo G, and Baas PW
Current Biology; 18(24):1972-1977 (Dec 23, 2008).

"The Microtubule-severing Proteins Spastin and Katanin Participate Differently in the Formation of Axonal Branches"
Yu W, Qiang L, Solowska JM, Karabay A, Korulu S, and Baas PW
Molecular Biology of the Cell;19(4):1485-1498 (Apr 2008).


Contact Information


Research Office

Department of Neurobiology & Anatomy
2900 W. Queen Lane
Philadelphia, PA 19129
Phone: 215.991.8298
Fax: 215.843.9082