Abstract—
Frontotemporal dementia is a progressive neurodegenerative disorder with high clinical, genetic, and pathomorphological diversity It is the third most common cause of dementia in all ages and the most common cause of early onset dementia (below 65). Despite its multifactorial nature, up to 40% of patients have a family history where the autosomal dominant inheritance type is seen in a quarter of cases. In this review, we describe key genes whose mutations can result in the development of frontotemporal dementia, the possible pathogenic mechanisms of the degenerative process, and provide information on the clinical features of the disease for different genetic variants. Special emphasis is placed on the frontotemporal dementia phenotype that is associated with amyotrophic lateral sclerosis.
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REFERENCES
Bang J., Spina S., Miller B.L. 2015. Frontotemporal dementia. Lancet. 386, 1672–1682.
Goldman J.S., Farmer J.M., Wood E.M., Johnson J.K., Boxer A., Neuhaus J., Lomen-Hoerth C., Wilhelmsen K.C., Lee V.M.Y., Grossman M., Miller B.L. 2005. Comparison of family histories in FTLD subtypes and related tauopathies. Neurology. 65, 1817–1819.
Rademakers R., Neumann M., Mackenzie I.R. 2012. Advances in understanding the molecular basis of frontotemporal dementia. Nat. Rev. Neurol. 8, 423–434.
Shi J., Shaw C.L., Plessis D.D., Richardson A.M.T., Bailey L.K., Julien C., Stopford C., Thompson J., Varma A., Craufurd D, Tian J., Pickering-Brown S., Neary D., Snowden J.S., Mann D.M.A. 2005. Histopathological changes underlying frontotemporal lobar degeneration with clinicopathological correlation. Acta Neuropathol.110, 501‒512.
Mackenzie I.R.A., Neumann M., Baborie A., Sampathu D.M., Plessis D.D., Jaros E., Perry R.H., Trojanowski J.Q., Mann D.M.A., Lee V.M.Y. 2011. A harmonized classification system for FTLD-TDP pathology. Acta Neuropathol.122, 111‒113.
Forman M.S., Farmer J., Johnson J.K., Clark C.M., Arnold S.E., Coslett H.B., Chatterjee A., Hurtig H.I., Karlawish J.H., Rosen H.J., Van Deerlin V., Lee V.M.Y., Miller B.L., Trojanowski J.Q., Grossman M. 2006. Frontotemporal dementia: Clinicopathological correlations. Ann. Neurol.59, 952‒962.
Josephs K.A., Hodges J.R., Snowden J.S., Mackenzie I.R., Neumann M., Mann D.M., Dickson D.W. 2011. Neuropathological background of phenotypical variability in frontotemporal dementia. Acta Neuropathol.122, 137‒153.
Rohrer J.D., Lashley T., Schott J.M., Warren J.E., Mead S., Isaacs A.M., Beck J., Hardy J., de Silva R., Warrington E., Troakes C., Al-Sarraj S., King A., Borroni B., Clarkson M.J., et al. 2011. Clinical and neuroanatomical signatures of tissue pathology in frontotemporal lobar degeneration. Brain.134, 2565‒2581.
Snowden J.S., Thompson J.C., Stopford C.L., Richardson A.M.T., Gerhard A., Neary D., Mann D.M.A. 2011. Clinical diagnosis of early-onset dementias: Diagnostic accuracy and clinico-pathological relationships. Brain.134, 2478‒2492.
Snowden J.S., Hu Q., Rollinson S., Halliwell N., Ro-binson A., Davidson Y.S., Momeni P., Baborie A., Griffiths T.D., Jaros E., Perry R.H., Richardson A., Pickering-Brown S.M., Neary D., Mann D.M.A. 2011. The most common type of FTLD-FUS (aFTLD-U) is associated with a distinct clinical form of frontotemporal dementia but is not related to mutations in the FUS gene. Acta Neuropathol.122, 99‒110.
Wilhelmsen K.C., Lynch T., Pavlou E., Higgins M., Nygaard T.G. 1994. Localization of disinhibition-dementia-parkinsonism-amyotrophy complex to 17q21-22. Am. J. Hum.Genet. 55, 1159–1165.
Lynch T., Sano M., Marder K.S., Bell K.L., Foster N.L., Defending R.F., Sima A.A.F., Keohane C., Nygaard T.G., Fahn S., Mayeux R., Rowland L.P., Wilhelmsen K.C. 1994. Clinical characteristics of a family with chromosome 17-linked disinhibition-dementia-parkinsonism-amyotrophy complex. Neurology.44, 1878–1884.
Hutton M., Lendon C.L., Rizzu P., Baker M., Froelich S., Houlden H., Pickering-Brown S., Chakraverty S., Isaacs A., Grover A., Hackett J., Adamson J., Lincoln S., Dickson D., Davies P., et al. 1998. Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17. Nature. 393, 702–705.
Wang Y., Mandelkow E. 2016. Tau in physiology and pathology. Nat. Rev. Neurosci. 17, 5–21.
Boeve B., Hutton M. 2008. Refining frontotemporal dementia with parkinsonism linked to chromosome 17: introducing FTDP-17 (MAPT. and FTDP-17 (PGRN). Arch. Neurol.65, 460–464.
Pickering-Brown S.M., Rollinson S., Plessis D., Morrison K.E., Varma A., Richardson A.M.T., Neary D., Snowden J.S., Mann D.M.A. 2008. Frequency and clinical characteristics of progranulin mutation carriers in the Manchester frontotemporal lobar degeneration cohort: Comparison with patients with MAPT and no known mutations. Brain.131, 721–731.
Rademakers R., Cruts M., Van Broeckhoven C. 2004. The role of tau (MAPT) in frontotemporal dementia and related tauopathies. Hum. Mutat.24, 277–295.
Malkani R., D’Souza I., Gwinn-Hardy K., Schellenberg G.D., Hardy J., Momeni P. 2006. A MAPT mutation in a regulatory element upstream of exon 10 causes frontotemporal dementia. Neurobiol. Dis.22, 401–403.
Hong M., Zhukareva V., Vogelsberg-Ragaglia V., Wszolek Z., Reed L., Miller B.I., Geschwind D.H., Bird T.D., McKeel D., Goate A., Morris J.C., Wilhelmsen K.C., Schellenberg G.D., Trojanowski J.Q., Lee V.M.Y. 1998. Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17. Science. 282, 1914–1917.
Goedert M., Jakes R., Crowther R.A. 1999. Effects of frontotemporal dementia FTDP-17 mutations on heparin-induced assembly of tau filaments. FEBS Lett.450, 306–311.
Rovelet-Lecrux A., Lecourtois M., Thomas-Anterion C., Le Ber I., Brice A., Frebourg T., Hannequin D., Campion D. 2009. Partial deletion of the MAPT gene: A novel mechanism of FTDP-17. Hum. Mutat.30, E591‒E602.
Rovelet-Lecrux A., Hannequin D., Guillin O., Legallic S., Jurici S., Wallon D., Frebourg T., Campion D. 2010. Frontotemporal dementia phenotype associated with MAPT gene duplication. J. Alzheimer’s Dis. 21, 897–902.
Mann D.M.A., Snowden J.S. 2017. Frontotemporal lobar degeneration: Pathogenesis, pathology and pathways to phenotype. Brain Pathol.27, 723–736.
Baker M., Mackenzie I.R., Pickering-Brown S.M., Gass J., Rademakers R., Lindholm C., Snowden J., Adamson J., Sadovnick A.D., Rollinson S., Cannon A., Dwosh E., Neary D., Melquist S., Richardson A., et al. 2006. Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17. Nature. 442, 916–919.
Cruts M., Gijselink I., Van Der Zee J., Engelborghs S., Wils H., Pirici D., Rademakers R., Vandenberghe R., Dermaut B., Martin J.J., van Duijn C., Peeters K., Sciot R., Santens P., De Pooter T., et al. 2006. Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21. Nature. 442, 920–924.
Petkau T.L., Leavitt B.R. 2014. Progranulin in neurodegenerative disease. Trends Neurosci.37, 388–398.
Hrabal R., Chen Z., James S., Bennett H.P., Ni F. 1996. The hairpin stack fold, a novel protein architecture for a new family of protein growth factors. Nat. Struct. Biol.3, 747–752.
Gass J., Cannon A., Mackenzie I.R., Boeve B., Baker M., Adamson J., Josephs K. 2006. Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration. Hum. Mol. Genet. 15, 2988–3001.
Yu C.E., Bird T.D., Bekris L.M., Montine T.J., Leverenz J.B., Steinbart E., Wood E.M. 2010. The spectrum of mutations in progranulin: A collaborative study screening 545 cases of neurodegeneration. Arch. Neurol. 67, 161–170.
Pietroboni A.M., Fumagalli G.G., Ghezzi L., Fenoglio C., Cortini F., Serpente M., Bassi M. 2011. Phenotypic heterogeneity of the GRN Asp22fs mutation in a large Italian kindred. J. Alzheimer’s Dis. 24, 253–259.
Neumann M., Sampathu D.M., Kwong L.K., Truax A.C., Micsenyi M.C., Chou T.T., McCluskey L.F. 2006. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science. 314, 130–133.
Smith K.R., Damiano J., Franceschetti S., Carpenter S., Canafoglia L., Morbin M., Sims, K.B. 2012. Strikingly different clinicopathological phenotypes determined by progranulin-mutation dosage. Am. J. Hum. Genet. 90, 1102–1107.
Mole S.E., Cotman S.L. 2015. Genetics of the neuronal ceroid lipofuscinoses (Batten disease). Biochim. Biophys. Acta–Mol.Basis Dis. 1852, 2237–2241.
Benussi A., Padovani A., Borroni B. 2015. Phenotypic heterogeneity of monogenic frontotemporal dementia. Front. Aging Neurosci. 7, 171.
Le Ber I., Camuzat A., Hannequin D., Pasquier F., Guedj E., Rovelet-Lecrux A., Puel M. 2008. Phenotype variability in progranulin mutation carriers: A clinical, neuropsychological, imaging and genetic study. Brain.131, 732–746.
Cerami C., Marcone A., Galimberti D., Villa C., Scarpini E., Cappa S.F. 2011. From genotype to phenotype: Two cases of genetic frontotemporal lobar degeneration with premorbid bipolar disorder. J. Alzheimer’s Dis.27, 791–797.
Ghidoni R., Benussi L., Glionna M., Franzoni M., Binetti G. 2008. Low plasma progranulin levels predict progranulin mutations in frontotemporal lobar degeneration. Neurology. 71, 1235–1239.
Carecchio M., Fenoglio C., De Riz M., Guidi I., Comi C., Cortini F., Monaco F. 2009. Progranulin plasma levels as potential biomarker for the identification of GRN deletion carriers. A case with atypical onset as clinical amnestic mild cognitive impairment converted to Alzheimer’s disease. J. Neurol. Sci.287, 291–293.
Hosler B., Siddique T., Sapp P.C., Sailor W., Huang M.C., Hossain A., Hung W.Y. 2000. Linkage of familial amyotrophic lateral to chromosome 9q21-q22. J. Am. Med. Assoc. 284, 1664–1669.
DeJesus-Hernandez M., Mackenzie I.R., Boeve B.F., Boxer A.L., Baker M., Rutherford N.J., Kouri N. 2011. Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS. Neuron. 72, 245–256.
Renton A.E., Majounie E., Waite A., Simón-Sánchez J., Rollinson S., Gibbs J.R., Kalimo H. 2011. A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD. Neuron.72, 257–268.
van Blitterswijk M., DeJesus-Hernandez M., Niemantsverdriet E., Murray M.E., Heckman M.G., Diehl N.N., Serrano G. 2013. Association between repeat sizes and clinical and pathological characteristics in carriers of C9ORF72 repeat expansions (Xpansize-72): A cross-sectional cohort study. Lancet Neurol.12, 978–988.
Ishiura H., Tsuji S. 2015. Epidemiology and molecular mechanism of frontotemporal lobar degeneration/amyotrophic lateral sclerosis with repeat expansion mutation in C9orf72.J. Neurogenet.29, 85–94.
Cooper-Knock J., Kirby J., Highley R., Shaw P.J. 2015. The spectrum of C9orf72-mediated neurodegeneration and amyotrophic lateral sclerosis. Neurotherapeutics. 12, 326–339.
Galimberti D., Fenoglio C., Serpente M., Villa C., Bonsi R., Arighi A., Clodomiro A. 2013. Autosomal dominant frontotemporal lobar degeneration due to the C9ORF72 hexanucleotide repeat expansion: late-onset psychotic clinical presentation. 2013. Biol. Psychiatry.74, 384–391.
Galimberti D., Reif A., Dell’Osso B., Palazzo C., Villa C., Fenoglio C., Paoli R.A. 2014. C9ORF72 hexanucleotide repeat expansion as a rare cause of bipolar disorder. Bipolar Disorders.16, 448–449.
Galimberti D., Reif A., Dell’Osso B., Kittel-Schneider S., Leonhard C., Herr A., Cioffi S.M. 2014. C9ORF72 hexanucleotide repeat expansion is a rare cause of schizophrenia. Neurobiol. Aging.35, 1214.e7‒1214.e10.
Majounie E., Abramzon Y., Renton A.E., Perry R., Bassett S.S., Pletnikova O., Traynor B.J. 2012. Repeat expansion in C9ORF72 in Alzheimer’s disease. N. Engl. J. Med.366, 283–284.
Gendron T.F., Bieniek K.F., Zhang Y.J., Jansen-West K., Ash P.E., Caulfield T., Cosio, D.M. 2013. Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS. Acta Neuropathol.126, 829–844.
Mori K., Arzberger T., Grässer F.A., Gijselinck I., May S., Rentzsch K., Van Broeckhoven C. 2013. Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins. Acta Neuropathol.126, 881–893.
Mizielinska S., Isaacs A.M. 2014. C9orf72 amyotrophic lateral sclerosis and frontotemporal dementia: Gain or loss of function? Curr. Opin. Neurol.27, 515–523.
Freibaum B.D., Lu Y., Lopez-Gonzalez R., Kim N.C., Almeida S., Lee K.H., Petrucelli L. 2015. GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport. Nature.525, 129–133.
May S., Hornburg D., Schludi M.H., Arzberger T., Rentzsch K., Schwenk B.M., Mann M. 2014. C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration. Acta Neuropathol.128, 485–503.
Lehmer C., Oeckl P., Weishaupt J.H., Volk A.E., Diehl-Schmid J., Schroeter M.L., Landwehrmeyer B. 2017. Poly-GP in cerebrospinal fluid links C9orf72-associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD. EMBO Mol. Med.9, 859–868.
Haeusler A.R., Donnelly C.J., Rothstein J.D. 2016. The expanding biology of the C9orf72 nucleotide repeat expansion in neurodegenerative disease. Nat. Rev. Neurosci.17, 383–395.
Reddy K., Zamiri B., Stanley S.Y., Macgregor R.B., Pearson C.E. 2013. The disease-associated r(GGGGCC)n repeat from the C9orf72 gene forms tract length-dependent uni- and multimolecular RNA G-quadruplex structures. J. Biol. Chem.288, 9860–9866.
Gijselinck I., Van Mossevelde S., van der Zee J., Sieben A., Engelborghs S., De Bleecker J., Heeman B. 2016. The C9orf72 repeat size correlates with onset age of disease, DNA methylation and transcriptional downregulation of the promoter. Mol. Psychiatry.21, 1112–1124.
Skibinski G., Parkinson N.J., Brown J.M., Chakrabarti L., Lloyd S.L., Hummerich H., Brandner S. 2005. Mutations in the endosomal ESCRTIII-complex subunit CHMP2B in frontotemporal dementia. Nat. Genet.37, P. 806.
Urwin H., Ghazi-Noori S., Collinge J., Isaacs A. 2009. The role of CHMP2B in frontotemporal dementia. Biochem. Soc. Transactions.37, 208–212.
Lindquist S.G., Brændgaard H., Svenstrup K., Isaacs A.M., Nielsen J.E., FReJA Consortium. 2008. Frontotemporal dementia linked to chromosome 3 (FTD-3)-current concepts and the detection of a previously unknown branch of the Danish FTD-3 family. Eur. J. Neurol.15, 667–670.
Urwin H., Authier A., Nielsen J.E., Metcalf D., Powell C., Froud K., Fisher E.M. 2010. Disruption of endocytic trafficking in frontotemporal dementia with CHMP2B mutations. Hum. Mol. Genet.19, 2228–2238.
M. Isaacs A., Johannsen P., Holm I., E. Nielsen J. 2011. Frontotemporal dementia caused by CHMP2B mutations. Curr. Alzheimer Res.8, 246–251.
Watts G.D.J., Wymer J., Kovach M.J., Mehta S.G., Mumm S., Darvish D., Kimonis V.E. 2004. Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia is caused by mutant valosin-containing protein. Nat. Genet.36, 377–381.
Kimonis V.E., Fulchiero E., Vesa J., Watts G. 2008. VCP disease associated with myopathy, Paget disease of bone and frontotemporal dementia: Review of a unique disorder. Biochim. Biophys. Acta (BBA)-Mol. Basis Dis.1782, 744‒748.
Mehta S.G., Khare M., Ramani R., Watts G.D.J., Simon M., Osann K.E., Donkervoort S., Dec E., Nalbandian A., Platt J., Pasquali M., Wang A., Mozaffar T., Smith C.D., Kimonis V.E. 2013. Genotype–phenotype studies of VCP-associated inclusion body myopathy with Paget disease of bone and/or frontotemporal dementia. Clin. Genet.83, 422‒431.
Spina S., Van Laar A.D., Murrell J.R., Hamilton R.L., Kofler J.K., Epperson F., Ghetti B. 2013. Phenotypic variability in three families with valosin-containing protein mutation. Eur. J. Neurol.20, 251–258.
Ju J.S., Weihl C.C. 2010. Inclusion body myopathy, Paget’s disease of the bone and fronto-temporal dementia: A disorder of autophagy. Hum. Mol. Genet.19, 38–45.
Ng A.S.L., Rademakers R., Miller B.L. 2015. Frontotemporal dementia: A bridge between dementia and neuromuscular disease. Ann. N.Y. Acad. Sci.1338, 71–93.
Rea S.L., Majcher V., Searle M.S., Layfield R. 2014. SQSTM1 mutations ‒ Bridging Paget disease of bone and ALS/FTLD. Exp. Cell Res.325, 27–37.
Bannwarth S., Ait-El-Mkadem S., Chaussenot A., Genin E.C., Lacas-Gervais S., Fragaki K., Verschueren A. 2014. A mitochondrial origin for frontotemporal dementia and amyotrophic lateral sclerosis through CHCHD10 involvement. Brain.137, 2329–2345.
Zhang M., Xi Z., Zinman L., Bruni A.C., Maletta R.G., Curcio S.A., Sorbi S. 2015. Mutation analysis of CHCHD10 in different neurodegenerative diseases. Brain.138, e380.
Perrone F., Nguyen, H.P., Van Mossevelde S., Moisse M., Sieben A., Santens P., Cras P. 2017. Investigating the role of ALS genes CHCHD10 and TUBA4A in Belgian FTD-ALS spectrum patients. Neurobiol. Aging.51, 177.e9‒177.e16.
Cirulli E.T., Lasseigne B.N., Petrovski S., Sapp P.C., Dion P.A., Leblond C.S., Ren Z. 2015. Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways. Science.347, 1436–1441.
Pottier C., Bieniek K.F., Finch N., van de Vorst M., Baker M., Perkersen R., DeTure M. 2016. Whole-genome sequencing reveals important role for TBK1 and OPTN mutations in frontotemporal lobar dementia without motor neuron disease. Acta Neuropathol. 130, 77–92.
Rainero I., Rubino E., Michelerio A., D’Agata F., Gentile S., Pinessi L. 2017. Recent advances in the molecular genetics of frontotemporal lobar degeneration. Funct. Neurol.32, 7‒16.
Neumann M., Valori C.F., Ansorge O., Kretzschmar H.A., Munoz D.G., Kusaka H., Mackenzie I.R. 2012. Transportin 1 accumulates specifically with FET proteins but no other transportin cargos in FTLD-FUS and is absent in FUS inclusions in ALS with FUS mutations. Acta Neuropathol.124, 705–716.
Dillen L., Van Langenhove T., Engelborghs S., Vandenbulcke M., Sarafov S., Tournev I., Jordanova A. 2013. Explorative genetic study of UBQLN2 and PFN1 in an extended Flanders-Belgian cohort of frontotemporal lobar degeneration patients. Neurobiol. Aging.34, 1711.e1‒1711.e5.
Deerlin V.M., Sleiman P.M., Martinez-Lage M., Chen-Plotkin A., Wang L.S., Graff-Radford N.R., Arnold S.E., Mann D.M.A., Pickering-Brown S.M., Seelaar H., Heutink P., van Swieten J.C., Murrell J.R., Ghetti B., Spina S., et al. 2010. Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP43 inclusions. Nat. Genet.42, 234–239.
Cruchaga C., Graff C., Chiang H.H., Wang J., Hinrichs A.L., Spiegel N., Goate A. 2011. Association of TMEM106B gene polymorphism with age at onset in granulin mutation carriers and plasma granulin protein levels. Arch. Neurol.68, 581–586.
Gallagher M.D., Suh E., Grossman M., Elman L., McCluskey L., Van Swieten, J.C., Rohrer J.D. 2014. TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions. Acta Neuropathol.127, 407–418.
Van Blitterswijk M., Mullen B., Nicholson A.M., Bieniek, K.F., Heckman M.G., Baker M.C., Hsiung G.Y.R. TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia. Acta Neuropathol.127, 397–406.
Brady O.A., Zheng Y., Murphy K., Huang M., Hu F. 2013. The frontotemporal lobar degeneration risk factor, TMEM106B, regulates lysosomal morphology and function. Hum. Mol. Genet.22, 685–695.
Rollinson S., Rohrer J.D., van der Zee J., Sleegers K., Mead S., Engelborghs S., Pickering-Brown S.M. 2011. No association of PGRN 3’UTR rs5848 in frontotemporal lobar degeneration. Neurobiol. Aging.32, 754–755.
Ferrari R., Hernandez D.G., Nalls M.A., Rohrer J.D., Ramasamy A., Kwok J.R. 2014. Frontotemporal dementia and its subtypes: A genome-wide association study. Lancet Neurol.13, 686–699.
Tsai R.M., Boxer A.L. 2016. Therapy and clinical trials in frontotemporal dementia: Past, present, and future. J. Neurochem.20, 211–221.
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The work is supported by The Russian Foundation for Basic Research (project no. 19-015-00533).
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Translated by A. Khaitin
Abbreviations: AD, Alzheimer’s disease; ALS, amyotrophic lateral sclerosis; FTD, frontotemporal dementia; bvFTD, behavioral variant FTD; PPA, primary progressive aphasia; svPPA, semantic variant PPA; avPPA, agrammatic variant PPA; FTD-ALS, FTD associated with amyotrophic lateral sclerosis (ALS); FTLD, frontotemporal lobar degeneration.
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Shpilyukova, Y.A., Fedotova, E.Y. & Illarioshkin, S.N. Genetic Diversity in Frontotemporal Dementia. Mol Biol 54, 13–23 (2020). https://doi.org/10.1134/S0026893320010136
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DOI: https://doi.org/10.1134/S0026893320010136