Stephen Strittmatter
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Research Summary
Neural Repair and Neuro-Degeneration
Neurological injury frequently interrupts connections while sparing nerve cells. Spinal Cord Injury (SCI) is the epitome of a disconnection syndrome, in which surviving neural tissue fails to function due to lost communication at the level of injury. For the organism to regain function, new pathways must form by growth of cut or surviving nerve fibers. Unfortunately, the growth of axons and the rearrangement of brain circuitry are extremely limited in the adult brain and spinal cord.
We focus on understanding the molecular pathways that limit fiber growth and functional rewiring of neuronal circuits during health and disease. Axonal growth encompasses both neural plasticity and repair. Technically, we utilize genome-wide functional screening, chronic in vivo imaging of neuronal connections, genetic alteration of mice and induction of surgical lesions resembling clinical SCI and Stroke. In particular, we have found that the NogoReceptor (NgR1) pathway mediating myelin inhibition of axonal growth plays a role in titrating anatomical plasticity in the adult CNS.
In Alzheimer's Disease and several other neurodegenerative conditions, nerve cells are lost over time. Molecular contributors to this pathology have been discovered by genetic methods, but their mechanism of action has remained poorly understood. We have focused on defining the pathophysiological action of Amyloid-beta (Aß) peptide oligomers in Alzheimer's Disease, and on the role of secreted Progranulin in Fronto-Temporal Dementia. For both of these molecules, interaction with the specific receptors on the neuronal surface is crucial. We utilize receptor ligand binding assays, expression cloning, electrophysiology, genetics and mouse behavior to study these pathways. Interrupting an Aß oligomer signal transduction pharamacologically rescues synapses and memory function in Alzheimer's disease models. These novel approaches are being translated to clinical trials.
Coauthors
Research Interests
Alzheimer Disease; Axons; Dementia; Spinal Cord Injuries; Regenerative Medicine; Frontotemporal Dementia
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Selected Publications
- Optic nerve regeneration screen identifies multiple genes restricting adult neural repair.Lindborg JA, Tran NM, Chenette DM, DeLuca K, Foli Y, Kannan R, Sekine Y, Wang X, Wollan M, Kim IJ, Sanes JR, Strittmatter SM. Optic nerve regeneration screen identifies multiple genes restricting adult neural repair. Cell Reports 2021, 34: 108777. PMID: 33657370, PMCID: PMC8009559, DOI: 10.1016/j.celrep.2021.108777.
- Fronto-temporal dementia risk gene TMEM106B has opposing effects in different lysosomal storage disorders.Perez-Canamas A, Takahashi H, Lindborg JA, Strittmatter SM. Fronto-temporal dementia risk gene TMEM106B has opposing effects in different lysosomal storage disorders. Brain Communications 2021, 3: fcaa200. PMID: 33796852, PMCID: PMC7990118, DOI: 10.1093/braincomms/fcaa200.
- Spreading of Alzheimer tau seeds is enhanced by aging and template matching with limited impact of amyloid-β.Nies SH, Takahashi H, Herber CS, Huttner A, Chase A, Strittmatter SM. Spreading of Alzheimer tau seeds is enhanced by aging and template matching with limited impact of amyloid-β. The Journal Of Biological Chemistry 2021, 297: 101159. PMID: 34480901, PMCID: PMC8477193, DOI: 10.1016/j.jbc.2021.101159.
- Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury.Wang X, Zhou T, Maynard GD, Terse PS, Cafferty WB, Kocsis JD, Strittmatter SM. Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury. Brain : A Journal Of Neurology 2020, 143: 1697-1713. PMID: 32375169, PMCID: PMC7850069, DOI: 10.1093/brain/awaa116.
- Fyn kinase inhibition reduces protein aggregation, increases synapse density and improves memory in transgenic and traumatic Tauopathy.Tang SJ, Fesharaki-Zadeh A, Takahashi H, Nies SH, Smith LM, Luo A, Chyung A, Chiasseu M, Strittmatter SM. Fyn kinase inhibition reduces protein aggregation, increases synapse density and improves memory in transgenic and traumatic Tauopathy. Acta Neuropathologica Communications 2020, 8: 96. PMID: 32611392, PMCID: PMC7329553, DOI: 10.1186/s40478-020-00976-9.
- Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in.Chiasseu M, Fesharaki A, Saito T, Saido TC, Strittmatter SM. Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in. Neurobiology Of Disease 2020, 145: 105059. PMID: 32858147, PMCID: PMC7572902, DOI: 10.1016/j.nbd.2020.105059.
- Rescue of Transgenic Alzheimer's Pathophysiology by Polymeric Cellular Prion Protein Antagonists.Gunther EC, Smith LM, Kostylev MA, Cox TO, Kaufman AC, Lee S, Folta-Stogniew E, Maynard GD, Um JW, Stagi M, Heiss JK, Stoner A, Noble GP, Takahashi H, Haas LT, Schneekloth JS, Merkel J, Teran C, Naderi ZK, Supattapone S, Strittmatter SM. Rescue of Transgenic Alzheimer's Pathophysiology by Polymeric Cellular Prion Protein Antagonists. Cell Reports 2019, 26: 145-158.e8. PMID: 30605671, PMCID: PMC6358723, DOI: 10.1016/j.celrep.2018.12.021.
- Pyk2 Signaling through Graf1 and RhoA GTPase Is Required for Amyloid-β Oligomer-Triggered Synapse Loss.Lee S, Salazar SV, Cox TO, Strittmatter SM. Pyk2 Signaling through Graf1 and RhoA GTPase Is Required for Amyloid-β Oligomer-Triggered Synapse Loss. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2019, 39: 1910-1929. PMID: 30626696, PMCID: PMC6407289, DOI: 10.1523/JNEUROSCI.2983-18.2018.
- Alzheimer's Disease Risk Factor Pyk2 Mediates Amyloid-β-Induced Synaptic Dysfunction and Loss.Salazar SV, Cox TO, Lee S, Brody AH, Chyung AS, Haas LT, Strittmatter SM. Alzheimer's Disease Risk Factor Pyk2 Mediates Amyloid-β-Induced Synaptic Dysfunction and Loss. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2019, 39: 758-772. PMID: 30518596, PMCID: PMC6343652, DOI: 10.1523/JNEUROSCI.1873-18.2018.
- Systematic and standardized comparison of reported amyloid-β receptors for sufficiency, affinity, and Alzheimer's disease relevance.Smith LM, Kostylev MA, Lee S, Strittmatter SM. Systematic and standardized comparison of reported amyloid-β receptors for sufficiency, affinity, and Alzheimer's disease relevance. The Journal Of Biological Chemistry 2019, 294: 6042-6053. PMID: 30787106, PMCID: PMC6463724, DOI: 10.1074/jbc.RA118.006252.
- Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma.Sekine Y, Algarate PT, Cafferty WBJ, Strittmatter SM. Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2019, 39: 3204-3216. PMID: 30804090, PMCID: PMC6788813, DOI: 10.1523/JNEUROSCI.2996-18.2019.
- Anti-PrPC antibody rescues cognition and synapses in transgenic alzheimer mice.Cox TO, Gunther EC, Brody AH, Chiasseu MT, Stoner A, Smith LM, Haas LT, Hammersley J, Rees G, Dosanjh B, Groves M, Gardener M, Dobson C, Vaughan T, Chessell I, Billinton A, Strittmatter SM. Anti-PrPC antibody rescues cognition and synapses in transgenic alzheimer mice. Annals Of Clinical And Translational Neurology 2019, 6: 554-574. PMID: 30911579, PMCID: PMC6414488, DOI: 10.1002/acn3.730.
- Effect of AZD0530 on Cerebral Metabolic Decline in Alzheimer Disease: A Randomized Clinical Trial.van Dyck CH, Nygaard HB, Chen K, Donohue MC, Raman R, Rissman RA, Brewer JB, Koeppe RA, Chow TW, Rafii MS, Gessert D, Choi J, Turner RS, Kaye JA, Gale SA, Reiman EM, Aisen PS, Strittmatter SM. Effect of AZD0530 on Cerebral Metabolic Decline in Alzheimer Disease: A Randomized Clinical Trial. JAMA Neurology 2019, 76: 1219-1229. PMID: 31329216, PMCID: PMC6646979, DOI: 10.1001/jamaneurol.2019.2050.
- Functional Genome-wide Screen Identifies Pathways Restricting Central Nervous System Axonal Regeneration.Sekine Y, Lin-Moore A, Chenette DM, Wang X, Jiang Z, Cafferty WB, Hammarlund M, Strittmatter SM. Functional Genome-wide Screen Identifies Pathways Restricting Central Nervous System Axonal Regeneration. Cell Reports 2018, 23: 415-428. PMID: 29642001, PMCID: PMC5937716, DOI: 10.1016/j.celrep.2018.03.058.
- Liquid and Hydrogel Phases of PrPC Linked to Conformation Shifts and Triggered by Alzheimer's Amyloid-β Oligomers.Kostylev MA, Tuttle MD, Lee S, Klein LE, Takahashi H, Cox TO, Gunther EC, Zilm KW, Strittmatter SM. Liquid and Hydrogel Phases of PrPC Linked to Conformation Shifts and Triggered by Alzheimer's Amyloid-β Oligomers. Molecular Cell 2018, 72: 426-443.e12. PMID: 30401430, PMCID: PMC6226277, DOI: 10.1016/j.molcel.2018.10.009.
- Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease.Salazar SV, Gallardo C, Kaufman AC, Herber CS, Haas LT, Robinson S, Manson JC, Lee MK, Strittmatter SM. Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2017, 37: 9207-9221. PMID: 28842420, PMCID: PMC5607466, DOI: 10.1523/JNEUROSCI.0722-17.2017.
- Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer's Mouse Phenotypes.Haas LT, Salazar SV, Smith LM, Zhao HR, Cox TO, Herber CS, Degnan AP, Balakrishnan A, Macor JE, Albright CF, Strittmatter SM. Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer's Mouse Phenotypes. Cell Reports 2017, 20: 76-88. PMID: 28683325, PMCID: PMC5547898, DOI: 10.1016/j.celrep.2017.06.023.
- Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice.Klein ZA, Takahashi H, Ma M, Stagi M, Zhou M, Lam TT, Strittmatter SM. Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice. Neuron 2017, 95: 281-296.e6. PMID: 28728022, PMCID: PMC5558861, DOI: 10.1016/j.neuron.2017.06.026.
- Metabotropic glutamate receptor 5 couples cellular prion protein to intracellular signalling in Alzheimer's disease.Haas LT, Salazar SV, Kostylev MA, Um JW, Kaufman AC, Strittmatter SM. Metabotropic glutamate receptor 5 couples cellular prion protein to intracellular signalling in Alzheimer's disease. Brain : A Journal Of Neurology 2016, 139: 526-46. PMID: 26667279, PMCID: PMC4840505, DOI: 10.1093/brain/awv356.
- Erasure of fear memories is prevented by Nogo Receptor 1 in adulthood.Bhagat SM, Butler SS, Taylor JR, McEwen BS, Strittmatter SM. Erasure of fear memories is prevented by Nogo Receptor 1 in adulthood. Molecular Psychiatry 2016, 21: 1281-9. PMID: 26619810, PMCID: PMC4887429, DOI: 10.1038/mp.2015.179.
- Fyn inhibition rescues established memory and synapse loss in Alzheimer mice.Kaufman AC, Salazar SV, Haas LT, Yang J, Kostylev MA, Jeng AT, Robinson SA, Gunther EC, van Dyck CH, Nygaard HB, Strittmatter SM. Fyn inhibition rescues established memory and synapse loss in Alzheimer mice. Annals Of Neurology 2015, 77: 953-71. PMID: 25707991, PMCID: PMC4447598, DOI: 10.1002/ana.24394.
- Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein.Um JW, Kaufman AC, Kostylev M, Heiss JK, Stagi M, Takahashi H, Kerrisk ME, Vortmeyer A, Wisniewski T, Koleske AJ, Gunther EC, Nygaard HB, Strittmatter SM. Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein. Neuron 2013, 79: 887-902. PMID: 24012003, PMCID: PMC3768018, DOI: 10.1016/j.neuron.2013.06.036.
- Anatomical plasticity of adult brain is titrated by Nogo Receptor 1.Akbik FV, Bhagat SM, Patel PR, Cafferty WB, Strittmatter SM. Anatomical plasticity of adult brain is titrated by Nogo Receptor 1. Neuron 2013, 77: 859-66. PMID: 23473316, PMCID: PMC3594793, DOI: 10.1016/j.neuron.2012.12.027.
- Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons.Um JW, Nygaard HB, Heiss JK, Kostylev MA, Stagi M, Vortmeyer A, Wisniewski T, Gunther EC, Strittmatter SM. Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons. Nature Neuroscience 2012, 15: 1227-35. PMID: 22820466, PMCID: PMC3431439, DOI: 10.1038/nn.3178.
- Recovery from chronic spinal cord contusion after Nogo receptor intervention.Wang X, Duffy P, McGee AW, Hasan O, Gould G, Tu N, Harel NY, Huang Y, Carson RE, Weinzimmer D, Ropchan J, Benowitz LI, Cafferty WB, Strittmatter SM. Recovery from chronic spinal cord contusion after Nogo receptor intervention. Annals Of Neurology 2011, 70: 805-21. PMID: 22162062, PMCID: PMC3238798, DOI: 10.1002/ana.22527.
- Sortilin-mediated endocytosis determines levels of the frontotemporal dementia protein, progranulin.Hu F, Padukkavidana T, Vægter CB, Brady OA, Zheng Y, Mackenzie IR, Feldman HH, Nykjaer A, Strittmatter SM. Sortilin-mediated endocytosis determines levels of the frontotemporal dementia protein, progranulin. Neuron 2010, 68: 654-67. PMID: 21092856, PMCID: PMC2990962, DOI: 10.1016/j.neuron.2010.09.034.
- Memory impairment in transgenic Alzheimer mice requires cellular prion protein.Gimbel DA, Nygaard HB, Coffey EE, Gunther EC, Laurén J, Gimbel ZA, Strittmatter SM. Memory impairment in transgenic Alzheimer mice requires cellular prion protein. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2010, 30: 6367-74. PMID: 20445063, PMCID: PMC3323924, DOI: 10.1523/JNEUROSCI.0395-10.2010.
- Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers.Laurén J, Gimbel DA, Nygaard HB, Gilbert JW, Strittmatter SM. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. Nature 2009, 457: 1128-32. PMID: 19242475, PMCID: PMC2748841, DOI: 10.1038/nature07761.
- Delayed Nogo receptor therapy improves recovery from spinal cord contusion.Wang X, Baughman KW, Basso DM, Strittmatter SM. Delayed Nogo receptor therapy improves recovery from spinal cord contusion. Annals Of Neurology 2006, 60: 540-9. PMID: 16958113, PMCID: PMC2855693, DOI: 10.1002/ana.20953.
- Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.McGee AW, Yang Y, Fischer QS, Daw NW, Strittmatter SM. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor. Science (New York, N.Y.) 2005, 309: 2222-6. PMID: 16195464, PMCID: PMC2856689, DOI: 10.1126/science.1114362.
- Nogo-66 receptor prevents raphespinal and rubrospinal axon regeneration and limits functional recovery from spinal cord injury.Kim JE, Liu BP, Park JH, Strittmatter SM. Nogo-66 receptor prevents raphespinal and rubrospinal axon regeneration and limits functional recovery from spinal cord injury. Neuron 2004, 44: 439-51. PMID: 15504325, DOI: 10.1016/j.neuron.2004.10.015.
- Blockade of Nogo-66, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein by soluble Nogo-66 receptor promotes axonal sprouting and recovery after spinal injury.Li S, Liu BP, Budel S, Li M, Ji B, Walus L, Li W, Jirik A, Rabacchi S, Choi E, Worley D, Sah DW, Pepinsky B, Lee D, Relton J, Strittmatter SM. Blockade of Nogo-66, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein by soluble Nogo-66 receptor promotes axonal sprouting and recovery after spinal injury. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2004, 24: 10511-20. PMID: 15548666, PMCID: PMC6730300, DOI: 10.1523/JNEUROSCI.2828-04.2004.
- Axon regeneration in young adult mice lacking Nogo-A/B.Kim JE, Li S, GrandPré T, Qiu D, Strittmatter SM. Axon regeneration in young adult mice lacking Nogo-A/B. Neuron 2003, 38: 187-99. PMID: 12718854, DOI: 10.1016/s0896-6273(03)00147-8.
- Nogo-66 receptor antagonist peptide promotes axonal regeneration.GrandPré T, Li S, Strittmatter SM. Nogo-66 receptor antagonist peptide promotes axonal regeneration. Nature 2002, 417: 547-51. PMID: 12037567, DOI: 10.1038/417547a.
- Myelin-associated glycoprotein as a functional ligand for the Nogo-66 receptor.Liu BP, Fournier A, GrandPré T, Strittmatter SM. Myelin-associated glycoprotein as a functional ligand for the Nogo-66 receptor. Science (New York, N.Y.) 2002, 297: 1190-3. PMID: 12089450, DOI: 10.1126/science.1073031.
- Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration.Fournier AE, GrandPre T, Strittmatter SM. Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration. Nature 2001, 409: 341-6. PMID: 11201742, DOI: 10.1038/35053072.
- Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein.GrandPré T, Nakamura F, Vartanian T, Strittmatter SM. Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein. Nature 2000, 403: 439-44. PMID: 10667797, DOI: 10.1038/35000226.
- Plexin-neuropilin-1 complexes form functional semaphorin-3A receptors.Takahashi T, Fournier A, Nakamura F, Wang LH, Murakami Y, Kalb RG, Fujisawa H, Strittmatter SM. Plexin-neuropilin-1 complexes form functional semaphorin-3A receptors. Cell 1999, 99: 59-69. PMID: 10520994, DOI: 10.1016/s0092-8674(00)80062-8.
- Neuropilin-1 extracellular domains mediate semaphorin D/III-induced growth cone collapse.Nakamura F, Tanaka M, Takahashi T, Kalb RG, Strittmatter SM. Neuropilin-1 extracellular domains mediate semaphorin D/III-induced growth cone collapse. Neuron 1998, 21: 1093-100. PMID: 9856464, DOI: 10.1016/s0896-6273(00)80626-1.
- Collapsin-induced growth cone collapse mediated by an intracellular protein related to UNC-33.Goshima Y, Nakamura F, Strittmatter P, Strittmatter SM. Collapsin-induced growth cone collapse mediated by an intracellular protein related to UNC-33. Nature 1995, 376: 509-14. PMID: 7637782, DOI: 10.1038/376509a0.
- Transcriptomic taxonomy and neurogenic trajectories of adult human, macaque, and pig hippocampal and entorhinal cells.Franjic D, Skarica M, Ma S, Arellano JI, Tebbenkamp ATN, Choi J, Xu C, Li Q, Morozov YM, Andrijevic D, Vrselja Z, Spajic A, Santpere G, Li M, Zhang S, Liu Y, Spurrier J, Zhang L, Gudelj I, Rapan L, Takahashi H, Huttner A, Fan R, Strittmatter SM, Sousa AMM, Rakic P, Sestan N. Transcriptomic taxonomy and neurogenic trajectories of adult human, macaque, and pig hippocampal and entorhinal cells. Neuron 2022, 110: 452-469.e14. PMID: 34798047, PMCID: PMC8813897, DOI: 10.1016/j.neuron.2021.10.036.
- NogoA-expressing astrocytes limit peripheral macrophage infiltration after ischemic brain injury in primates.Boghdadi AG, Spurrier J, Teo L, Li M, Skarica M, Cao B, Kwan WC, Merson TD, Nilsson SK, Sestan N, Strittmatter SM, Bourne JA. NogoA-expressing astrocytes limit peripheral macrophage infiltration after ischemic brain injury in primates. Nature Communications 2021, 12: 6906. PMID: 34824275, PMCID: PMC8617297, DOI: 10.1038/s41467-021-27245-0.
- Translational PET Imaging of Spinal Cord Injury with the Serotonin Transporter Tracer [11C]AFM.Fang H, Rossano S, Wang X, Nabulsi N, Kelley B, Fowles K, Ropchan J, Strittmatter SM, Carson RE, Huang Y. Translational PET Imaging of Spinal Cord Injury with the Serotonin Transporter Tracer [11C]AFM. Molecular Imaging And Biology : MIB : The Official Publication Of The Academy Of Molecular Imaging 2022 PMID: 35020138, DOI: 10.1007/s11307-021-01698-7.
- PET Imaging of Synaptic Density: Challenges and Opportunities of Synaptic Vesicle Glycoprotein 2A PET in Small Animal Imaging.Toyonaga T, Fesharaki-Zadeh A, Strittmatter SM, Carson RE, Cai Z. PET Imaging of Synaptic Density: Challenges and Opportunities of Synaptic Vesicle Glycoprotein 2A PET in Small Animal Imaging. Frontiers In Neuroscience 2022, 16: 787404. PMID: 35345546, PMCID: PMC8957200, DOI: 10.3389/fnins.2022.787404.
- An unexpected protein aggregate in diseased and ageing brains.Takahashi H, Strittmatter SM. An unexpected protein aggregate in diseased and ageing brains. Nature 2022, 605: 227-228. PMID: 35379977, DOI: 10.1038/d41586-022-00873-2.
- Rabphilin3A reduces integrin-dependent growth cone signaling to restrict axon regeneration after trauma.Sekine Y, Kannan R, Wang X, Strittmatter SM. Rabphilin3A reduces integrin-dependent growth cone signaling to restrict axon regeneration after trauma. Experimental Neurology 2022, 353: 114070. PMID: 35398339, DOI: 10.1016/j.expneurol.2022.114070.
- Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy.Brody AH, Nies SH, Guan F, Smith LM, Mukherjee B, Salazar SA, Lee S, Lam TKT, Strittmatter SM. Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy. Molecular Neurodegeneration 2022, 17: 32. PMID: 35501917, PMCID: PMC9063299, DOI: 10.1186/s13024-022-00526-y.
Clinical Trials
Conditions | Study Title |
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Men's Health; Women's Health | Evaluating the Safety, Tolerability, Pharmacokinetics and Receptor Occupancy of BMS-984923 |