Marion Buckwalter

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Marion Buckwalter
Marion Buckwalter at the World Economic Forum.jpg
Buckwalter in 2015
NationalityAmerican
Alma materUniversity of Chicago
University of Michigan
University of California San Francisco
Known forNeuroimmune response to stroke
AwardsGeorge R. DeMuth Medical Scientist Award for Excellence, American Academy of Neurology Annual Meeting Scholarship
Scientific career
FieldsNeuroimmunology, neurology
InstitutionsStanford University School of Medicine

Marion Buckwalter is an American neurologist and neuroscientist and Professor of Neurology and Neurosurgery at the Stanford University School of Medicine. Buckwalter studies how inflammatory responses affect brain recovery after injury or insult, with a specific emphasis on the neuroimmune and glial cell response after stroke.

Contents

Early life and education

In 1984, Buckwalter pursued her undergraduate degree in biological chemistry at the University of Chicago, in Illinois. [1] She completed her Bachelors of Science in 1988 and then pursued her MD/PhD training at the University of Michigan in Ann Arbor in the Department of Human Genetics. [1] Under the mentorship of Sally Camper, Buckwalter helped to localize specific disease causing mutations to mouse chromosomes. [2] She completed her dual degree training in 1996, and then pursued further clinical training at the University of California, San Francisco. [3] Buckwalter completed her Internship in Medicine and Residency in Neurology at the UCSF Medical Center, becoming a Board Certified in Neurology and Psychiatry in 2001. [3] Buckwalter then conducted her Fellowship training in Neurological Critical Care at UCSF, completing her training in 2002. [3]

From 2002 to 2004, Buckwalter conducted her postdoctoral fellowship in Neurology and Neurological Sciences at Stanford University School of Medicine. [4] Under the mentorship of Tony Wyss-Coray, Buckwalter explored the impacts of brain inflammation and neuroimmune signalling in brain disease. [2]

Localization and identification of mouse mutations

During her Ph.D. at the University of Michigan, Buckwalter localized various genes in the mouse genome. She first identified the location of Ames dwarf (df) mutation on mouse chromosome 11 via an intersubspecific backcross. [5] Buckwalter and her colleagues then mapped, for the first time, the location of the Gabrg-2 subunit of the GABA receptor as well as interferon regulatory factor 1 on mouse chromosome 11. [6] Following this, Buckwalter mapped the candidate genes of the spasmodic recessive mutation to mouse chromosome 11 and evaluated the candidate mutated genes leading to the behavioral abnormalities associated with the mutation such as fine motor tremors, leg clasping, and stiffness. [7] She found, through recombination analyses, that the spasmodic mutation maps to the Glra1 gene, coding for a glycine receptor subunit, and this point mutation decreases the glycine receptor function. [8]

Effects of transforming growth factor signalling in the central nervous system

Much of Buckwalter's postdoctoral research focused on exploring the effects of transforming growth factor beta (TGFb) signalling in the brain. [9] Human data showing increases in TGFb mRNA correlating with the degree of cerebrovascular amyloid deposition in the brain prompted Buckwalter to explore how TGFb might be implicated in cerebrovascular pathology in disease. [9] She found that overexpression of TGFb in astrocytes lead to Alzheimer's Disease like abnormalities and it led to decreased cerebral blood flow in the limbic system. [9]

Since TGFb is also rapidly increased in aging and after injury, Buckwalter and her colleagues proposed that it may play a role in decreasing hippocampal neurogenesis. [10] They found that over-expression of TGFb in astrocytes almost completely blocked neurogenesis in the hippocampus and it appears to exert its effects at very early stages in neurogenesis, before differentiation into either neurons or astrocytes. [10]

Buckwalter and her colleagues later explored how TGF affects T cell recruitment to the brain meninges and parenchyma in models of Alzheimer's disease. [11] They found that the increased TFGb in addition to increases in amyloid precursor protein led to increased CD4+ T cell infiltration. [11]

Career and research

In 2004, Buckwalter became an instructor in the Department of Neurology and Neurological Sciences at Stanford University. [4] By 2007, she was promoted to Assistant Professor. In 2015, she was promoted to Associate Professor, and in 2020, to full Professor. Buckwalter holds the title of Professor in the Department of Neurology and Neurological Sciences and is a Bio-X Affiliated Faculty. [4] Buckwalter is a leader in stroke research and directs several clinical stroke initiatives at Stanford. She is the deputy director of the Wu Tsai Neurosciences Institute, co-founded and now co-leads the Stroke Collaborative Action Network, and is the co-founder of the Stroke Recovery Program at Stanford. [12]

Buckwalter is also the Principal Investigator of the Buckwalter Lab. [13] Her lab focuses on exploring the neuroimmune landscape after brain insult and injury to guide stroke recovery treatments and therapeutic development. [13] Buckwalter explores how astrocytes regulate inflammation in the brain after stroke, how transforming growth factor beta (TGFb) signalling can limit the immune responses after brain injury and infection, and the central and peripheral effects of stroke on the immune system. [13]

Role of TGFb in brain inflammation

In her lab at Stanford, Buckwalter has been exploring the pleiotropic nature of TGFb in the brain post-stroke. [14] TGFb appears to be neuroprotective after stroke through orchestrating glial scarring and regulating the local immune landscape in the brain, so Buckwalter and her lab wanted to see how this process changes in age. [14]  They found that activated macrophages and microglia were the predominant sources of TGFb after stroke and that astrocytes, macrophages, and microglia all upregulate their TGFb dependent signalling after stroke whereas neurons and oligodendrocytes do not. [14] Moreover, the increases in TGFb signalling increase with age. [14]

Further exploration of the effects of this over-expression highlighted the striking effects that TGFb can have on the neural landscape in the long term. [15] Along with Sheena Josselyn and Paul Frankland, Buckwalter helped to discover that TGFb led to volumetric expansion in the hippocampus which was associated with defects in spatial learning. [15]

In the context of infection, however, TGFb appears to play a critical role in moderating the immune response. [16] Buckwalter and her colleagues showed that upon infection with Toxoplasma gondii , TGFb is critical to preventing over-infiltration of immune cells and actually helps to limit neuronal injury and death. [16] Similarly, after an acute stroke, astrocyte mediated TGFb signalling appeared to limit neuroinflammation and preserve brain function. [17] The acute astrocytic responses to TFGb seem to mediate the brain's anti-inflammatory response to stroke. [17]

Small molecule stroke treatment

Buckwalter and her colleague Frank Longo developed a small molecule tropomyosin-related kinase B agonist (LM22A-4) and tested its effects on stroke recovery. [18] They found that LM22A-4 promoted neurogenesis when administered 3 days post-stroke and it significantly improved recovery, improving limb speed and accelerating the return to normal gate accuracy. [18]

Stroke effects

To explore the underlying causes of post-stroke associated dementia, Buckwalter probed the B lymphocyte response to stroke that had been observed. [19] She found that B lymphocytes infiltrate the brain and are found in neuropil and are associated with aberrant LTP and cognitive delays. [19] Further, pharmacologically blocking B lymphocytes prevented cognitive delays after stroke. [19]  To look at the possibility of B cell mediated deficits in cognition in humans, Buckwalter and her colleagues measured autoantibodies in patients after stroke and found that increases in autoantibodies to myelin basic protein were associated with cognitive decline after stroke. [20]

Awards and honors

Select publications

Related Research Articles

<span class="mw-page-title-main">Glia</span> Support cells in the nervous system

Glia, also called glial cells (gliocytes) or neuroglia, are non-neuronal cells in the central nervous system and the peripheral nervous system that do not produce electrical impulses. The neuroglia make up more than one half the volume of neural tissue in the human body. They maintain homeostasis, form myelin in the peripheral nervous system, and provide support and protection for neurons. In the central nervous system, glial cells include oligodendrocytes, astrocytes, ependymal cells and microglia, and in the peripheral nervous system they include Schwann cells and satellite cells.

<span class="mw-page-title-main">Astrocyte</span> Type of brain cell

Astrocytes, also known collectively as astroglia, are characteristic star-shaped glial cells in the brain and spinal cord. They perform many functions, including biochemical control of endothelial cells that form the blood–brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, regulation of cerebral blood flow, and a role in the repair and scarring process of the brain and spinal cord following infection and traumatic injuries. The proportion of astrocytes in the brain is not well defined; depending on the counting technique used, studies have found that the astrocyte proportion varies by region and ranges from 20% to around 40% of all glia. Another study reports that astrocytes are the most numerous cell type in the brain. Astrocytes are the major source of cholesterol in the central nervous system. Apolipoprotein E transports cholesterol from astrocytes to neurons and other glial cells, regulating cell signaling in the brain. Astrocytes in humans are more than twenty times larger than in rodent brains, and make contact with more than ten times the number of synapses.

<span class="mw-page-title-main">Astrogliosis</span> Increase in astrocytes in response to brain injury

Astrogliosis is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or neurodegenerative disease. In healthy neural tissue, astrocytes play critical roles in energy provision, regulation of blood flow, homeostasis of extracellular fluid, homeostasis of ions and transmitters, regulation of synapse function and synaptic remodeling. Astrogliosis changes the molecular expression and morphology of astrocytes, in response to infection for example, in severe cases causing glial scar formation that may inhibit axon regeneration.

<span class="mw-page-title-main">Glial fibrillary acidic protein</span> Type III intermediate filament protein

Glial fibrillary acidic protein (GFAP) is a protein that is encoded by the GFAP gene in humans. It is a type III intermediate filament (IF) protein that is expressed by numerous cell types of the central nervous system (CNS), including astrocytes and ependymal cells during development. GFAP has also been found to be expressed in glomeruli and peritubular fibroblasts taken from rat kidneys, Leydig cells of the testis in both hamsters and humans, human keratinocytes, human osteocytes and chondrocytes and stellate cells of the pancreas and liver in rats.

<span class="mw-page-title-main">Rostral migratory stream</span> One path neural stem cells take to reach the olfactory bulb


The rostral migratory stream (RMS) is a specialized migratory route found in the brain of some animals along which neuronal precursors that originated in the subventricular zone (SVZ) of the brain migrate to reach the main olfactory bulb (OB). The importance of the RMS lies in its ability to refine and even change an animal's sensitivity to smells, which explains its importance and larger size in the rodent brain as compared to the human brain, as our olfactory sense is not as developed. This pathway has been studied in the rodent, rabbit, and both the squirrel monkey and rhesus monkey. When the neurons reach the OB they differentiate into GABAergic interneurons as they are integrated into either the granule cell layer or periglomerular layer.

<span class="mw-page-title-main">Neuroimmune system</span>

The neuroimmune system is a system of structures and processes involving the biochemical and electrophysiological interactions between the nervous system and immune system which protect neurons from pathogens. It serves to protect neurons against disease by maintaining selectively permeable barriers, mediating neuroinflammation and wound healing in damaged neurons, and mobilizing host defenses against pathogens.

Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes. In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar.

Neural stem cells (NSCs) are self-renewing, multipotent cells that firstly generate the radial glial progenitor cells that generate the neurons and glia of the nervous system of all animals during embryonic development. Some neural progenitor stem cells persist in highly restricted regions in the adult vertebrate brain and continue to produce neurons throughout life. Differences in the size of the central nervous system are among the most important distinctions between the species and thus mutations in the genes that regulate the size of the neural stem cell compartment are among the most important drivers of vertebrate evolution.

<span class="mw-page-title-main">Radial glial cell</span> Bipolar-shaped progenitor cells of all neurons in the cerebral cortex and some glia

Radial glial cells, or radial glial progenitor cells (RGPs), are bipolar-shaped progenitor cells that are responsible for producing all of the neurons in the cerebral cortex. RGPs also produce certain lineages of glia, including astrocytes and oligodendrocytes. Their cell bodies (somata) reside in the embryonic ventricular zone, which lies next to the developing ventricular system.

<span class="mw-page-title-main">Glia limitans</span> Thin astrocyte membrane surrounding the brain and spinal cord

The glia limitans, or the glial limiting membrane, is a thin barrier of astrocyte foot processes associated with the parenchymal basal lamina surrounding the brain and spinal cord. It is the outermost layer of neural tissue, and among its responsibilities is the prevention of the over-migration of neurons and neuroglia, the supporting cells of the nervous system, into the meninges. The glia limitans also plays an important role in regulating the movement of small molecules and cells into the brain tissue by working in concert with other components of the central nervous system (CNS) such as the blood–brain barrier (BBB).

<span class="mw-page-title-main">Subventricular zone</span> Region outside each lateral ventricle of the brain

The subventricular zone (SVZ) is a region situated on the outside wall of each lateral ventricle of the vertebrate brain. It is present in both the embryonic and adult brain. In embryonic life, the SVZ refers to a secondary proliferative zone containing neural progenitor cells, which divide to produce neurons in the process of neurogenesis. The primary neural stem cells of the brain and spinal cord, termed radial glial cells, instead reside in the ventricular zone (VZ).

<span class="mw-page-title-main">Subgranular zone</span>

The subgranular zone (SGZ) is a brain region in the hippocampus where adult neurogenesis occurs. The other major site of adult neurogenesis is the subventricular zone (SVZ) in the brain.

Gliotransmitters are chemicals released from glial cells that facilitate neuronal communication between neurons and other glial cells. They are usually induced from Ca2+ signaling, although recent research has questioned the role of Ca2+ in gliotransmitters and may require a revision of the relevance of gliotransmitters in neuronal signalling in general.

Epileptogenesis is the gradual process by which a typical brain develops epilepsy. Epilepsy is a chronic condition in which seizures occur. These changes to the brain occasionally cause neurons to fire in an abnormal, hypersynchronous manner, known as a seizure.

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References

  1. 1 2 "Marion S. Buckwalter, MD, PhD". The Michael J. Fox Foundation for Parkinson's Research | Parkinson's Disease. Retrieved 2020-05-17.
  2. 1 2 "Marion S Buckwalter - Google Scholar Citations". scholar.google.com. Retrieved 2020-05-17.
  3. 1 2 3 "Marion S. Buckwalter, MD, PhD". stanfordhealthcare.org. Retrieved 2020-05-17.
  4. 1 2 3 4 5 6 7 "Biographical Sketch Buckwalter, Marion". Stanford.edu/Profiles. Retrieved May 15, 2020.
  5. ↑ Buckwalter, Marion S.; Katz, Ronald W.; Camper, Sally A. (July 1991). "Localization of the panhypopituitary dwarf mutation (df) on mouse chromosome 11 in an intersubspecific backross". Genomics. 10 (3): 515–526. doi:10.1016/0888-7543(91)90430-M. hdl: 2027.42/29261 . ISSN   0888-7543. PMID   1889803.
  6. ↑ Buckwalter, Marion S.; Lossie, Amy C.; Scarlett, Lori M.; Camper, Sally A. (1992-10-01). "Localization of the human Chromosome 5q genes Gabra-1, Gabrg-2, Il-4, Il-5, and Irf-1 on mouse Chromosome 11". Mammalian Genome. 3 (10): 604–607. doi:10.1007/BF00350629. hdl: 2027.42/46991 . ISSN   1432-1777. PMID   1358285. S2CID   30300461.
  7. ↑ Buckwalter, Marion S.; Testa, Claudia M.; Noebels, Jeffrey L.; Camper, Sally A. (August 1993). "Genetic Mapping and Evaluation of Candidate Genes for Spasmodic, a Neurological Mouse Mutation with Abnormal Startle Response". Genomics. 17 (2): 279–286. doi:10.1006/geno.1993.1322. hdl: 2027.42/30658 . ISSN   0888-7543. PMID   8406478.
  8. ↑ Buckwalter, M. S. (1997). "Localization of the Ames dwarf mutation and identification of the spasmodic and oscillator mutations": 1.{{cite journal}}: Cite journal requires |journal= (help)
  9. 1 2 3 Buckwalter, Marion; Pepper, Jon-Paul; Gaertner, Roger F.; Euw, Dominique Von; Lacombe, Pierre; Wyss-Coraya, Tony (2002). "Molecular and Functional Dissection of TGF-β1-Induced Cerebrovascular Abnormalities in Transgenic Mice". Annals of the New York Academy of Sciences. 977 (1): 87–95. Bibcode:2002NYASA.977...87B. doi:10.1111/j.1749-6632.2002.tb04801.x. ISSN   1749-6632. PMID   12480736. S2CID   21137605.
  10. 1 2 Buckwalter, Marion S.; Yamane, Makiko; Coleman, Bronwen S.; Ormerod, Brandi K.; Chin, Jocelyn T.; Palmer, Theo; Wyss-Coray, Tony (2006-07-01). "Chronically Increased Transforming Growth Factor-β1 Strongly Inhibits Hippocampal Neurogenesis in Aged Mice". The American Journal of Pathology. 169 (1): 154–164. doi:10.2353/ajpath.2006.051272. ISSN   0002-9440. PMC   1698757 . PMID   16816369.
  11. 1 2 Buckwalter, Marion S.; Coleman, Bronwen S.; Buttini, Manuel; Barbour, Robin; Schenk, Dale; Games, Dora; Seubert, Peter; Wyss-Coray, Tony (2006-11-01). "Increased T Cell Recruitment to the CNS after Amyloid β1–42 Immunization in Alzheimer's Mice Overproducing Transforming Growth Factor-β1". Journal of Neuroscience. 26 (44): 11437–11441. doi:10.1523/JNEUROSCI.2436-06.2006. ISSN   0270-6474. PMC   1892201 . PMID   17079673.
  12. ↑ "Internationally Recognized Neurologist Will Share Her Insights on the Aftermath of Stroke". The Independent. Retrieved 2020-05-17.
  13. 1 2 3 "Buckwalter Lab Research". Buckwalter Lab. Retrieved 2020-05-17.
  14. 1 2 3 4 Doyle, Kristian P.; Cekanaviciute, Egle; Mamer, Lauren E.; Buckwalter, Marion S. (2010-10-11). "TGFβ signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke". Journal of Neuroinflammation. 7 (1): 62. doi: 10.1186/1742-2094-7-62 . ISSN   1742-2094. PMC   2958905 . PMID   20937129.
  15. 1 2 Martinez-Canabal, Alonso; Wheeler, Anne L.; Sarkis, Dani; Lerch, Jason P.; Lu, Wei-Yang; Buckwalter, Marion S.; Wyss-Coray, Tony; Josselyn, Sheena A.; Frankland, Paul W. (2013). "Chronic over-expression of TGFβ1 alters hippocampal structure and causes learning deficits". Hippocampus. 23 (12): 1198–1211. doi:10.1002/hipo.22159. ISSN   1098-1063. PMID   23804429. S2CID   17941044.
  16. 1 2 Cekanaviciute, Egle; Dietrich, Hans K.; Axtell, Robert C.; Williams, Aaron M.; Egusquiza, Riann; Wai, Karen M.; Koshy, Anita A.; Buckwalter, Marion S. (2014-07-01). "Astrocytic TGF-β Signaling Limits Inflammation and Reduces Neuronal Damage during Central Nervous System Toxoplasma Infection". The Journal of Immunology. 193 (1): 139–149. doi:10.4049/jimmunol.1303284. ISSN   0022-1767. PMC   4075480 . PMID   24860191.
  17. 1 2 Cekanaviciute, Egle; Fathali, Nancy; Doyle, Kristian P.; Williams, Aaron M.; Han, Jullet; Buckwalter, Marion S. (2014). "Astrocytic transforming growth factor-beta signaling reduces subacute neuroinflammation after stroke in mice". Glia. 62 (8): 1227–1240. doi:10.1002/glia.22675. ISSN   1098-1136. PMC   4061255 . PMID   24733756.
  18. 1 2 Han Jullet; Pollak Julia; Yang Tao; Siddiqui Mohammad R.; Doyle Kristian P.; Taravosh-Lahn Kereshmeh; Cekanaviciute Egle; Han Alex; Goodman Jeremy Z.; Jones Britta; Jing Deqiang (2012-07-01). "Delayed Administration of a Small Molecule Tropomyosin-Related Kinase B Ligand Promotes Recovery After Hypoxic–Ischemic Stroke". Stroke. 43 (7): 1918–1924. doi:10.1161/STROKEAHA.111.641878. PMC   3383889 . PMID   22535263.
  19. 1 2 3 Doyle, Kristian P.; Quach, Lisa N.; Solé, Montse; Axtell, Robert C.; Nguyen, Thuy-Vi V.; Soler-Llavina, Gilberto J.; Jurado, Sandra; Han, Jullet; Steinman, Lawrence; Longo, Frank M.; Schneider, Julie A. (2015-02-04). "B-Lymphocyte-Mediated Delayed Cognitive Impairment following Stroke". The Journal of Neuroscience. 35 (5): 2133–2145. doi:10.1523/JNEUROSCI.4098-14.2015. ISSN   0270-6474. PMC   4315838 . PMID   25653369.
  20. ↑ Becker, Kyra J.; Tanzi, Patricia; Zierath, Dannielle; Buckwalter, Marion S. (2016-06-15). "Antibodies to myelin basic protein are associated with cognitive decline after stroke". Journal of Neuroimmunology. 295–296: 9–11. doi:10.1016/j.jneuroim.2016.04.001. ISSN   0165-5728. PMC   4884610 . PMID   27235342.
  21. ↑ "$9.6 million grant to fund research on vascular risk factors for brain aging, dementia". News Center. Retrieved 2020-05-17.
  22. 1 2 3 4 5 6 7 8 9 10 "Buckwalter Lab Publications". Buckwalter Lab. Retrieved 2020-05-17.
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