Immunotherapy with an antibody against CD1d modulates neuroinflammation in an α-synuclein transgenic model of Lewy body like disease.

Adaptive immunity Dementia with Lewy bodies Innate immunity Parkinson’s disease T cell α-synuclein

Journal

Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974

Informations de publication

Date de publication:
15 Apr 2024
Historique:
received: 20 12 2023
accepted: 01 04 2024
medline: 16 4 2024
pubmed: 16 4 2024
entrez: 15 4 2024
Statut: epublish

Résumé

The neuroinflammatory process in synucleinopathies of the aging population such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB) involves microglial activation as well as infiltration of the CNS by T cells and natural killer T cells (NKTs). To evaluate the potential of targeting NKT cells to modulate neuroinflammation, we treated α-syn transgenic (tg) mice (e.g.: Thy1 promoter line 61) with an antibody against CD1d, which is a glycoprotein expressed in antigen presenting cells (APCs). CD1d-presented lipid antigens activate NKT cells through the interaction with T cell receptor in NKTs, resulting in the production of cytokines. Thus, we hypothesized that blocking the APC-NKT interaction with an anti-CD1d antibody might reduce neuroinflammation and neurodegeneration in models of DLB/PD. Treatment with the anti-CD1d antibody did not have effects on CD3 (T cells), slightly decreased CD4 and increased CD8 lymphocytes in the mice. Moreover, double labeling studies showed that compared to control (IgG) treated α-syn tg mice, treatment with anti-CD1d decreased numbers of CD3/interferon γ (IFN γ)-positive cells, consistent with NKTs. Further double labeling studies showed that CD1d-positive cells co-localized with the astrocytes marker GFAP and that anti-CD1d antibody reduced this effect. While in control α-syn tg mice CD3 positive cells were near astrocytes, this was modified by the treatment with the CD1d antibody. By qPCR, levels of IFN γ, CCL4, and interleukin-6 were increased in the IgG treated α-syn tg mice. Treatment with CD1d antibody blunted this cytokine response that was associated with reduced astrocytosis and microgliosis in the CNS of the α-syn tg mice treated with CD1d antibody. Flow cytometric analysis of immune cells in α-syn tg mice revealed that CD1d-tet + T cells were also increased in the spleen of α-syn tg mice, which treatment with the CD1d antibody reduced. Reduced neuroinflammation in the anti-CD1d-treated α-syn tg mice was associated with amelioration of neurodegenerative pathology. These results suggest that reducing infiltration of NKT cells with an antibody against CD1d might be a potential therapeutical approach for DLB/PD.

Identifiants

pubmed: 38622654
doi: 10.1186/s12974-024-03087-7
pii: 10.1186/s12974-024-03087-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

93

Informations de copyright

© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.

Références

Iwai A, Masliah E, Yoshimoto M, Ge N, Flanagan L, de Silva HA, Kittel A, Saitoh T. The precursor protein of non-A beta component of Alzheimer’s disease amyloid is a presynaptic protein of the central nervous system. Neuron. 1995;14:467–75.
pubmed: 7857654 doi: 10.1016/0896-6273(95)90302-X
Shameli A, Xiao W, Zheng Y, Shyu S, Sumodi J, Meyerson HJ, Harding CV, Maitta RW. A critical role for alpha-synuclein in development and function of T lymphocytes. Immunobiology. 2016;221:333–40.
pubmed: 26517968 doi: 10.1016/j.imbio.2015.10.002
Ettle B, Kuhbandner K, Jorg S, Hoffmann A, Winkler J, Linker RA. Alpha-synuclein deficiency promotes neuroinflammation by increasing Th1 cell-mediated immune responses. J Neuroinflammation. 2016;13:201.
pubmed: 27565429 pmcid: 5002168 doi: 10.1186/s12974-016-0694-4
Sommer A, Fadler T, Dorfmeister E, Hoffmann AC, Xiang W, Winner B, Prots I. Infiltrating T lymphocytes reduce myeloid phagocytosis activity in synucleinopathy model. J Neuroinflammation. 2016;13:174.
pubmed: 27364890 pmcid: 4929755 doi: 10.1186/s12974-016-0632-5
Spillantini MG, Goedert M. The alpha-synucleinopathies: Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. Ann N Y Acad Sci. 2000;920:16–27.
pubmed: 11193145 doi: 10.1111/j.1749-6632.2000.tb06900.x
McKeith IG, Boeve BF, Dickson DW, Halliday G, Taylor JP, Weintraub D, Aarsland D, Galvin J, Attems J, Ballard CG, et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium. Neurology. 2017;89:88–100.
pubmed: 28592453 pmcid: 5496518 doi: 10.1212/WNL.0000000000004058
Alafuzoff I, Hartikainen P. Alpha-synucleinopathies. Handb Clin Neurol. 2017;145:339–53.
pubmed: 28987181 doi: 10.1016/B978-0-12-802395-2.00024-9
Savica R, Boeve BF, Mielke MM. When do alpha-synucleinopathies start? An Epidemiological Timeline: a review. JAMA Neurol. 2018;75:503–9.
pubmed: 29459985 doi: 10.1001/jamaneurol.2017.4243
Tansey MG, Wallings RL, Houser MC, Herrick MK, Keating CE, Joers V. Inflammation and immune dysfunction in Parkinson disease. Nat Rev Immunol. 2022;22:657–73.
pubmed: 35246670 pmcid: 8895080 doi: 10.1038/s41577-022-00684-6
Kim C, Ho DH, Suk JE, You S, Michael S, Kang J, Joong Lee S, Masliah E, Hwang D, Lee HJ, Lee SJ. Neuron-released oligomeric alpha-synuclein is an endogenous agonist of TLR2 for paracrine activation of microglia. Nat Commun. 2013;4:1562.
pubmed: 23463005 doi: 10.1038/ncomms2534
Kim C, Spencer B, Rockenstein E, Yamakado H, Mante M, Adame A, Fields JA, Masliah D, Iba M, Lee HJ, et al. Immunotherapy targeting toll-like receptor 2 alleviates neurodegeneration in models of synucleinopathy by modulating alpha-synuclein transmission and neuroinflammation. Mol Neurodegener. 2018;13:43.
pubmed: 30092810 pmcid: 6085656 doi: 10.1186/s13024-018-0276-2
Fiebich BL, Batista CRA, Saliba SW, Yousif NM, de Oliveira ACP. Role of Microglia TLRs in Neurodegeneration. Front Cell Neurosci. 2018;12:329.
pubmed: 30333729 pmcid: 6176466 doi: 10.3389/fncel.2018.00329
Caplan IF, Maguire-Zeiss KA. Toll-like receptor 2 signaling and current approaches for therapeutic modulation in Synucleinopathies. Front Pharmacol. 2018;9:417.
pubmed: 29780321 pmcid: 5945810 doi: 10.3389/fphar.2018.00417
Rostami J, Fotaki G, Sirois J, Mzezewa R, Bergstrom J, Essand M, Healy L, Erlandsson A. Astrocytes have the capacity to act as antigen-presenting cells in the Parkinson’s disease brain. J Neuroinflammation. 2020;17:119.
pubmed: 32299492 pmcid: 7164247 doi: 10.1186/s12974-020-01776-7
Sulzer D, Alcalay RN, Garretti F, Cote L, Kanter E, Agin-Liebes J, Liong C, McMurtrey C, Hildebrand WH, Mao X, et al. T cells from patients with Parkinson’s disease recognize alpha-synuclein peptides. Nature. 2017;546:656–61.
pubmed: 28636593 pmcid: 5626019 doi: 10.1038/nature22815
Iba M, Kim C, Sallin M, Kwon S, Verma A, Overk C, Rissman RA, Sen R, Sen JM, Masliah E. Neuroinflammation is associated with infiltration of T cells in Lewy body disease and alpha-synuclein transgenic models. J Neuroinflammation. 2020;17:214.
pubmed: 32680537 pmcid: 7368752 doi: 10.1186/s12974-020-01888-0
Gate D, Tapp E, Leventhal O, Shahid M, Nonninger TJ, Yang AC, Strempfl K, Unger MS, Fehlmann T, Oh H, et al. CD4(+) T cells contribute to neurodegeneration in Lewy body dementia. Science. 2021;374:868–74.
pubmed: 34648304 pmcid: 9122025 doi: 10.1126/science.abf7266
Subleski J, Weiss JM, Wiltrout RH, Ortaldo JR. Chapter Nineteen - NK and NKT cells: The innate–adaptive interface including humoral responses. In Natural Killer Cells Edited by Lotze MT, Thomson AW: Academic Press; 2010: 255–277.
Cui Y, Wan Q. NKT cells in neurological diseases. Front Cell Neurosci. 2019;13:245.
pubmed: 31231193 pmcid: 6558384 doi: 10.3389/fncel.2019.00245
Chen Y-J, Liao H-F. NK/NKT cells and aging. Int J Gerontol. 2007;1:65–76.
doi: 10.1016/S1873-9598(08)70025-5
Taniguchi M, Seino K, Nakayama T. The NKT cell system: bridging innate and acquired immunity. Nat Immunol. 2003;4:1164–5.
pubmed: 14639465 doi: 10.1038/ni1203-1164
Nair S, Dhodapkar MV. Natural killer T cells in Cancer Immunotherapy. Front Immunol. 2017;8:1178.
pubmed: 29018445 pmcid: 5614937 doi: 10.3389/fimmu.2017.01178
Holbrook J, Patel B, Camacho M, Kahanawita L, Greenland J, Williams-Gray CH. Natural killer cells have an activated profile in early Parkinson’s disease. J Neuroimmunol. 2023;382:578154.
pubmed: 37549558 doi: 10.1016/j.jneuroim.2023.578154
Barral DC, Brenner MB. CD1 antigen presentation: how it works. Nat Rev Immunol. 2007;7:929–41.
pubmed: 18037897 doi: 10.1038/nri2191
Rossjohn J, Pellicci DG, Patel O, Gapin L, Godfrey DI. Recognition of CD1d-restricted antigens by natural killer T cells. Nat Rev Immunol. 2012;12:845–57.
pubmed: 23154222 pmcid: 3740582 doi: 10.1038/nri3328
Watson MB, Richter F, Lee SK, Gabby L, Wu J, Masliah E, Effros RB, Chesselet MF. Regionally-specific microglial activation in young mice over-expressing human wildtype alpha-synuclein. Exp Neurol. 2012;237:318–34.
pubmed: 22750327 pmcid: 3443323 doi: 10.1016/j.expneurol.2012.06.025
Chesselet MF, Richter F, Zhu C, Magen I, Watson MB, Subramaniam SR. A progressive mouse model of Parkinson’s disease: the Thy1-aSyn (line 61) mice. Neurotherapeutics. 2012;9:297–314.
pubmed: 22350713 pmcid: 3337020 doi: 10.1007/s13311-012-0104-2
Rabl R, Breitschaedel C, Flunkert S, Duller S, Amschl D, Neddens J, Niederkofler V, Rockenstein E, Masliah E, Roemer H, Hutter-Paier B. Early start of progressive motor deficits in line 61 alpha-synuclein transgenic mice. BMC Neurosci. 2017;18:22.
pubmed: 28143405 pmcid: 5282838 doi: 10.1186/s12868-017-0341-8
Rockenstein E, Mallory M, Hashimoto M, Song D, Shults CW, Lang I, Masliah E. Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and Thy-1 promoters. J Neurosci Res. 2002;68:568–78.
pubmed: 12111846 doi: 10.1002/jnr.10231
Kim C, Beilina A, Smith N, Li Y, Kim M, Kumaran R, Kaganovich A, Mamais A, Adame A, Iba M et al. LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies. Sci Transl Med 2020, 12.
Halder RC, Jahng A, Maricic I, Kumar V. Mini review: immune response to myelin-derived sulfatide and CNS-demyelination. Neurochem Res. 2007;32:257–62.
pubmed: 17006761 doi: 10.1007/s11064-006-9145-4
Knieke K, Lingel H, Chamaon K, Brunner-Weinzierl MC. Migration of Th1 lymphocytes is regulated by CD152 (CTLA-4)-mediated signaling via PI3 kinase-dependent akt activation. PLoS ONE. 2012;7:e31391.
pubmed: 22412835 pmcid: 3295805 doi: 10.1371/journal.pone.0031391
Heneka MT, Golenbock DT, Latz E. Innate immunity in Alzheimer’s disease. Nat Immunol. 2015;16:229–36.
pubmed: 25689443 doi: 10.1038/ni.3102
Mayne K, White JA, McMurran CE, Rivera FJ, de la Fuente AG. Aging and neurodegenerative disease: is the adaptive Immune System a friend or foe? Front Aging Neurosci. 2020;12:572090.
pubmed: 33173502 pmcid: 7538701 doi: 10.3389/fnagi.2020.572090
Molteni M, Rossetti C. Neurodegenerative diseases: the immunological perspective. J Neuroimmunol. 2017;313:109–15.
pubmed: 29153601 doi: 10.1016/j.jneuroim.2017.11.002
Labzin LI, Heneka MT, Latz E. Innate immunity and neurodegeneration. Annu Rev Med. 2018;69:437–49.
pubmed: 29106805 doi: 10.1146/annurev-med-050715-104343
Gendelman HE, Mosley RL. A perspective on roles played by Innate and adaptive immunity in the pathobiology of neurodegenerative disorders. J Neuroimmune Pharmacol. 2015;10:645–50.
pubmed: 26520433 pmcid: 4662620 doi: 10.1007/s11481-015-9639-4
Rodrigues MC, Sanberg PR, Cruz LE, Garbuzova-Davis S. The innate and adaptive immunological aspects in neurodegenerative diseases. J Neuroimmunol. 2014;269:1–8.
pubmed: 24161471 doi: 10.1016/j.jneuroim.2013.09.020
Dressman D, Elyaman W. T cells: a growing Universe of roles in neurodegenerative diseases. Neuroscientist. 2022;28:335–48.
pubmed: 34160330 doi: 10.1177/10738584211024907
Allen Reish HE, Standaert DG. Role of alpha-synuclein in inducing innate and adaptive immunity in Parkinson disease. J Parkinsons Dis. 2015;5:1–19.
pubmed: 25588354 pmcid: 4405142 doi: 10.3233/JPD-140491
Kannarkat GT, Boss JM, Tansey MG. The role of innate and adaptive immunity in Parkinson’s disease. J Parkinsons Dis. 2013;3:493–514.
pubmed: 24275605 pmcid: 4102262 doi: 10.3233/JPD-130250
Chen Z, Chen S, Liu J. The role of T cells in the pathogenesis of Parkinson’s disease. Prog Neurobiol. 2018;169:1–23.
pubmed: 30114440 doi: 10.1016/j.pneurobio.2018.08.002
Williams GP, Schonhoff AM, Jurkuvenaite A, Gallups NJ, Standaert DG, Harms AS. CD4 T cells mediate brain inflammation and neurodegeneration in a mouse model of Parkinson’s disease. Brain. 2021;144:2047–59.
pubmed: 33704423 pmcid: 8370411 doi: 10.1093/brain/awab103
Faunce DE, Gamelli RL, Choudhry MA, Kovacs EJ. A role for CD1d-restricted NKT cells in injury-associated T cell suppression. J Leukoc Biol. 2003;73:747–55.
pubmed: 12773507 doi: 10.1189/jlb.1102540
Schneider DF, Palmer JL, Tulley JM, Kovacs EJ, Gamelli RL, Faunce DE. Prevention of NKT cell activation accelerates cutaneous wound closure and alters local inflammatory signals. J Surg Res. 2011;171:361–73.
pubmed: 21067780 doi: 10.1016/j.jss.2010.03.030
Lameris R, de Bruin RC, van Bergen En Henegouwen PM, Verheul HM, Zweegman S, de Gruijl TD, van der Vliet HJ. Generation and characterization of CD1d-specific single-domain antibodies with distinct functional features. Immunology. 2016;149:111–21.
pubmed: 27312006 pmcid: 4981610 doi: 10.1111/imm.12635
Nambiar J, Clarke AW, Shim D, Mabon D, Tian C, Windloch K, Buhmann C, Corazon B, Lindgren M, Pollard M, et al. Potent neutralizing anti-CD1d antibody reduces lung cytokine release in primate asthma model. MAbs. 2015;7:638–50.
pubmed: 25751125 pmcid: 4623119 doi: 10.1080/19420862.2015.1016693
Rayapudi M, Rajavelu P, Zhu X, Kaul A, Niranjan R, Dynda S, Mishra A, Mattner J, Zaidi A, Dutt P, Mishra A. Invariant natural killer T-cell neutralization is a possible novel therapy for human eosinophilic esophagitis. Clin Transl Immunol. 2014;3:e9.
doi: 10.1038/cti.2013.13
Chen X, Wang X, Keaton JM, Reddington F, Illarionov PA, Besra GS, Gumperz JE. Distinct endosomal trafficking requirements for presentation of autoantigens and exogenous lipids by human CD1d molecules. J Immunol. 2007;178:6181–90.
pubmed: 17475845 doi: 10.4049/jimmunol.178.10.6181
Zhang Y, Fung ITH, Sankar P, Chen X, Robison LS, Ye L, D’Souza SS, Salinero AE, Kuentzel ML, Chittur SV, et al. Depletion of NK cells improves cognitive function in the Alzheimer Disease Mouse Model. J Immunol. 2020;205:502–10.
pubmed: 32503894 doi: 10.4049/jimmunol.2000037
Kumar V, Delovitch TL. Different subsets of natural killer T cells may vary in their roles in health and disease. Immunology. 2014;142:321–36.
pubmed: 24428389 pmcid: 4080948 doi: 10.1111/imm.12247
Liu X, Li L, Si F, Huang L, Zhao Y, Zhang C, Hoft DF, Peng G. NK and NKT cells have distinct properties and functions in cancer. Oncogene. 2021;40:4521–37.
pubmed: 34120141 doi: 10.1038/s41388-021-01880-9
Krijgsman D, Hokland M, Kuppen PJK. The role of natural killer T cells in Cancer-A Phenotypical and Functional Approach. Front Immunol. 2018;9:367.
pubmed: 29535734 pmcid: 5835336 doi: 10.3389/fimmu.2018.00367
Paul S, Lal G. The molecular mechanism of natural killer cells function and its importance in Cancer Immunotherapy. Front Immunol. 2017;8:1124.
pubmed: 28955340 pmcid: 5601256 doi: 10.3389/fimmu.2017.01124
Maghazachi AA. On the role of natural killer cells in neurodegenerative diseases. Toxins (Basel). 2013;5:363–75.
pubmed: 23430541 doi: 10.3390/toxins5020363
Jadidi-Niaragh F, Shegarfi H, Naddafi F, Mirshafiey A. The role of natural killer cells in Alzheimer’s disease. Scand J Immunol. 2012;76:451–6.
pubmed: 22889057 doi: 10.1111/j.1365-3083.2012.02769.x
Solerte SB, Fioravanti M, Pascale A, Ferrari E, Govoni S, Battaini F. Increased natural killer cell cytotoxicity in Alzheimer’s disease may involve protein kinase C dysregulation. Neurobiol Aging. 1998;19:191–9.
pubmed: 9661993 doi: 10.1016/S0197-4580(98)00050-5
Earls RH, Menees KB, Chung J, Gutekunst CA, Lee HJ, Hazim MG, Rada B, Wood LB, Lee JK. NK cells clear alpha-synuclein and the depletion of NK cells exacerbates synuclein pathology in a mouse model of alpha-synucleinopathy. Proc Natl Acad Sci U S A. 2020;117:1762–71.
pubmed: 31900358 pmcid: 6983411 doi: 10.1073/pnas.1909110117
Zhang L, Zhang Y, Fan D. Pathological role of natural killer cells in Parkinson’s Disease: a systematic review. Front Aging Neurosci. 2022;14:890816.
pubmed: 35663564 pmcid: 9157643 doi: 10.3389/fnagi.2022.890816
Snyder-Cappione JE, Tincati C, Eccles-James IG, Cappione AJ, Ndhlovu LC, Koth LL, Nixon DF. A comprehensive ex vivo functional analysis of human NKT cells reveals production of MIP1-alpha and MIP1-beta, a lack of IL-17, and a Th1-bias in males. PLoS ONE. 2010;5:e15412.
pubmed: 21082024 pmcid: 2972714 doi: 10.1371/journal.pone.0015412
Deshmane SL, Kremlev S, Amini S, Sawaya BE. Monocyte chemoattractant protein-1 (MCP-1): an overview. J Interferon Cytokine Res. 2009;29:313–26.
pubmed: 19441883 pmcid: 2755091 doi: 10.1089/jir.2008.0027
Chang TT, Chen JW. Emerging role of chemokine CC motif ligand 4 related mechanisms in diabetes mellitus and cardiovascular disease: friends or foes? Cardiovasc Diabetol. 2016;15:117.
pubmed: 27553774 pmcid: 4995753 doi: 10.1186/s12933-016-0439-9
Takahashi T, Kim MS, Iwai-Shimada M, Fujimura M, Toyama T, Naganuma A, Hwang GW. Chemokine CCL4 Induced in Mouse Brain has a protective role against Methylmercury Toxicity. Toxics 2018, 6.
Overk CR, Masliah E. Pathogenesis of synaptic degeneration in Alzheimer’s disease and Lewy body disease. Biochem Pharmacol. 2014;88:508–16.
pubmed: 24462903 pmcid: 3973539 doi: 10.1016/j.bcp.2014.01.015
Rocha EM, De Miranda B, Sanders LH. Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson’s disease. Neurobiol Dis. 2018;109:249–57.
pubmed: 28400134 doi: 10.1016/j.nbd.2017.04.004
Spillantini MG, Goedert M. Neurodegeneration and the ordered assembly of alpha-synuclein. Cell Tissue Res. 2018;373:137–48.
pubmed: 29119326 doi: 10.1007/s00441-017-2706-9
Villar-Pique A, Lopes da Fonseca T, Outeiro TF. Structure, function and toxicity of alpha-synuclein: the Bermuda triangle in synucleinopathies. J Neurochem. 2016;139(Suppl 1):240–55.
pubmed: 26190401 doi: 10.1111/jnc.13249
Cocchi F, DeVico AL, Garzino-Demo A, Arya SK, Gallo RC, Lusso P. Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8 + T cells. Science. 1995;270:1811–5.
pubmed: 8525373 doi: 10.1126/science.270.5243.1811
Nuovo GJ, Alfieri ML. AIDS dementia is associated with massive, activated HIV-1 infection and concomitant expression of several cytokines. Mol Med. 1996;2:358–66.
pubmed: 8784788 pmcid: 2230156 doi: 10.1007/BF03401633

Auteurs

Michiyo Iba (M)

Laboratory of Neurogenetics, Molecular Neuropathology Unit, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.

Somin Kwon (S)

Laboratory of Neurogenetics, Molecular Neuropathology Unit, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.

Changyoun Kim (C)

Laboratory of Neurogenetics, Molecular Neuropathology Unit, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.

Marcell Szabo (M)

Laboratory of Neurogenetics, Molecular Neuropathology Unit, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.

Liam Horan-Portelance (L)

Laboratory of Neurogenetics, Molecular Neuropathology Unit, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.

Maria Lopez-Ocasio (M)

Flow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Pradeep Dagur (P)

Flow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Cassia Overk (C)

Department of Neurosciences, University of California, San Diego, La Jolla, CA, 92093, USA.

Robert A Rissman (RA)

Department of Neurosciences, University of California, San Diego, La Jolla, CA, 92093, USA.

Eliezer Masliah (E)

Laboratory of Neurogenetics, Molecular Neuropathology Unit, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA. eliezer.masliah@nih.gov.
Division of Neuroscience, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20814, USA. eliezer.masliah@nih.gov.

Classifications MeSH