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Precision Medicine for Frontotemporal Dementia

Liu, Mu-N, Lau, Chi-Ieong, Lin, Ching-Po·2019·Frontiers in Psychiatry
DOI 10.3389/fpsyt.2019.00075PMC PMC6393374
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Figure 1 Patterns of brain atrophy in clinical subtypes of frontotemporal dementia (7–9). (A) Areas of brain atrophy in behavioral-variant frontotemporal dementia (blue), right hemisphere lateral view; (B) Areas of brain atrophy in semantic-variant primary progressive aphasia(green), left hemisphere lateral view; (C) Areas of brain atrophy in non-fluent variant primary progressive aphasia, left hemisphere lateral view.
Figure 1 Patterns of brain atrophy in clinical subtypes of frontotemporal dementia (7–9). (A) Areas of brain atrophy in behavioral-variant frontotemporal dementia (blue), right hemisphere lateral view; (B) Areas of brain atrophy in semantic-variant primary progressive aphasia(green), left hemisphere lateral view; (C) Areas of brain atrophy in non-fluent variant primary progressive aphasia, left hemisphere lateral view.CC BY · PubMed Central
Figure 2 Clinical, pathological, and genetic associations in FTD (7–9, 37). Clinical symptoms are shown at left, colored regions of clinical diagnosis represent relative percentages of patients found to have each underlying neuropathological diagnosis. Blue line, genetic and pathological aspects of bvFTD; gray line, genetic, and pathological aspects of nfvPPA; purple line, genetic, and pathological aspects of svPPA. bvFTD, behavioral-variant frontotemporal dementia; svPPA, semantic-variant primary progressive aphasia; nfvPPA, non-fluent variant primary progressive aphasia; FUS, fused in sarcoma; TDP-43, transactive response (TAR) DNA-binding protein of 43 kDa; C9orf72, chromosome 9 open reading frame 72; GRN, progranulin mutations; MAPT, microtubule-associated protein tau; and VCP, valosin-containing protein.
Figure 2 Clinical, pathological, and genetic associations in FTD (7–9, 37). Clinical symptoms are shown at left, colored regions of clinical diagnosis represent relative percentages of patients found to have each underlying neuropathological diagnosis. Blue line, genetic and pathological aspects of bvFTD; gray line, genetic, and pathological aspects of nfvPPA; purple line, genetic, and pathological aspects of svPPA. bvFTD, behavioral-variant frontotemporal dementia; svPPA, semantic-variant primary progressive aphasia; nfvPPA, non-fluent variant primary progressive aphasia; FUS, fused in sarcoma; TDP-43, transactive response (TAR) DNA-binding protein of 43 kDa; C9orf72, chromosome 9 open reading frame 72; GRN, progranulin mutations; MAPT, microtubule-associated protein tau; and VCP, valosin-containing protein.CC BY · PubMed Central

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Research works printed but not linked: 101

  1. Pick, 1892, Über die Beziehungen der senilen Hirnatrophie zur Aphasie, Prager Med Wochenschr., 17, 165
  2. Alzheimer, 1911, Über eigenartige Krankheitsfälle der späteren Alters, Z Gesamte Neurol Psychiatr., 4, 356, 10.1007/BF02866241 · DOI
  3. Mesulam, 2001, Primary progressive aphasia, Ann Neurol., 49, 425, 10.1002/ana.91 · DOI
  4. Rascovsky, 2011, Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia, Brain, 134, 2456, 10.1093/brain/awr179 · DOI · Paper page
  5. Gorno-Tempini, 2011, Classification of primary progressive aphasia and its variants, Neurology, 76, 1006, 10.1212/WNL.0b013e31821103e6 · DOI · Paper page
  6. Elahi, 2017, A clinicopathological approach to the diagnosis of dementia, Nat Rev Neurol., 13, 457, 10.1038/nrneurol.2017.96 · DOI
  7. Bang, 2015, Frontotemporal dementia, Lancet, 386, 1672, 10.1016/S0140-6736(15)00461-4 · DOI · Paper page
  8. Olney, 2017, Frontotemporal dementia, Neurol Clin., 35, 339, 10.1016/j.ncl.2017.01.008 · DOI · Paper page
  9. Gordon, 2016, Advances in neuroimaging in frontotemporal dementia, J Neurochem., 138, 193, 10.1111/jnc.13656 · DOI
  10. Irwin, 2015, Frontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine, Acta Neuropathol., 129, 469, 10.1007/s00401-014-1380-1 · DOI
  11. Forman, 2006, Frontotemporal dementia: clinicopathological correlations, Ann Neurol., 59, 952, 10.1002/ana.20873 · DOI · Paper page
  12. Young, 2018, Frontotemporal dementia: latest evidence and clinical implications, Ther Adv Psychopharmacol., 8, 33, 10.1177/2045125317739818 · DOI
  13. Rogalski, 2014, Asymmetry of cortical decline in subtypes of primary progressive aphasia, Neurology, 83, 1184, 10.1212/WNL.0000000000000824 · DOI
  14. Rankin, 2008, Spontaneous social behaviors discriminate behavioral dementias from psychiatric disorders and other dementias, J Clin Psychiatry, 69, 60, 10.4088/JCP.v69n0109 · DOI
  15. Velakoulis, 2009, Frontotemporal dementia presenting as schizophrenia-like psychosis in young people: clinicopathological series and review of cases, Br J Psychiatry, 194, 298, 10.1192/bjp.bp.108.057034 · DOI
  16. Sha, 2012, Frontotemporal dementia due to C9ORF72 mutations: clinical and imaging features, Neurology, 79, 1002, 10.1212/WNL.0b013e318268452e · DOI
  17. Gorno-Tempini, 2008, The logopenic/phonological variant of primary progressive aphasia, Neurology, 71, 1227, 10.1212/01.wnl.0000320506.79811.da · DOI
  18. Kramer, 2003, Distinctive neuropsychological patterns in frontotemporal dementia, semantic dementia, and Alzheimer disease, Cogn Behav Neurol., 16, 211, 10.1097/00146965-200312000-00002 · DOI
  19. Josephs, 2006, Clinicopathological and imaging correlates of progressive aphasia and apraxia of speech, Brain, 129, 1385, 10.1093/brain/awl078 · DOI
  20. Burrell, 2011, Motor neuron dysfunction in frontotemporal dementia, Brain, 134, 2582, 10.1093/brain/awr195 · DOI
  21. Le Ber, 2006, Demographic, neurological and behavioural characteristics and brain perfusion SPECT in frontal variant of frontotemporal dementia, Brain, 129, 3051, 10.1093/brain/awl288 · DOI · Paper page
  22. Hoglinger, 2017, Clinical diagnosis of progressive supranuclear palsy: the movement disorder society criteria, Mov Disord., 32, 853, 10.1002/mds.26987 · DOI
  23. Litvan, 1996, Clinical research criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome): report of the NINDS-SPSP international workshop, Neurology, 47, 1, 10.1212/WNL.47.1.1 · DOI · Paper page
  24. Rosen, 2005, Neuroanatomical correlates of behavioural disorders in dementia, Brain, 128, 2612, 10.1093/brain/awh628 · DOI · Paper page
  25. Diehl-Schmid, 2014, Imaging frontotemporal lobar degeneration, Curr Neurol Neurosci Rep., 14, 489, 10.1007/s11910-014-0489-x · DOI
  26. Seeley, 2005, The natural history of temporal variant frontotemporal dementia, Neurology, 64, 1384, 10.1212/01.WNL.0000158425.46019.5C · DOI
  27. Tu, 2016, Divergent longitudinal propagation of white matter degradation in logopenic and semantic variants of primary progressive aphasia, J Alzheimers Dis., 49, 853, 10.3233/JAD-150626 · DOI
  28. Thompson, 2003, Left/right asymmetry of atrophy in semantic dementia: behavioral-cognitive implications, Neurology, 61, 1196, 10.1212/01.WNL.0000091868.28557.B8 · DOI
  29. Chan, 2009, The clinical profile of right temporal lobe atrophy, Brain, 132, 1287, 10.1093/brain/awp037 · DOI · Paper page
  30. Gorno-Tempini, 2004, Cognition and anatomy in three variants of primary progressive aphasia, Ann Neurol., 55, 335, 10.1002/ana.10825 · DOI
  31. Galantucci, 2011, White matter damage in primary progressive aphasias: a diffusion tensor tractography study, Brain, 134, 3011, 10.1093/brain/awr099 · DOI
  32. Struyfs, 2015, Cerebrospinal fluid P-Tau181P: biomarker for improved differential dementia diagnosis, Front Neurol., 6, 138, 10.3389/fneur.2015.00138 · DOI
  33. Josephs, 2011, Neuropathological background of phenotypical variability in frontotemporal dementia, Acta Neuropathol., 122, 137, 10.1007/s00401-011-0839-6 · DOI
  34. Lee, 2011, Clinicopathological correlations in corticobasal degeneration, Ann Neurol., 70, 327, 10.1002/ana.22424 · DOI · Paper page
  35. Bhardwaj, 2013, Characterizing TDP-43 interaction with its RNA targets, Nucleic Acids Res., 41, 5062, 10.1093/nar/gkt189 · DOI
  36. Neumann, 2006, Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis, Science, 314, 130, 10.1126/science.1134108 · DOI · Paper page
  37. Lee, 2011, Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration, Nat Rev Neurosci., 13, 38, 10.1038/nrn3121 · DOI · Paper page
  38. Mackenzie, 2011, Distinct pathological subtypes of FTLD-FUS, Acta Neuropathol., 121, 207, 10.1007/s00401-010-0764-0 · DOI
  39. Riedl, 2014, Frontotemporal lobar degeneration: current perspectives, Neuropsychiatr Dis Treat., 10, 297, 10.2147/NDT.S38706 · DOI
  40. Rohrer, 2009, The heritability and genetics of frontotemporal lobar degeneration, Neurology, 73, 1451, 10.1212/WNL.0b013e3181bf997a · DOI · Paper page
  41. Rademakers, 2012, Advances in understanding the molecular basis of frontotemporal dementia, Nat Rev Neurol., 8, 423, 10.1038/nrneurol.2012.117 · DOI
  42. DeJesus-Hernandez, 2011, Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS, Neuron, 72, 245, 10.1016/j.neuron.2011.09.011 · DOI · Paper page
  43. Hutton, 1998, Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17, Nature, 393, 702, 10.1038/31508 · DOI · Paper page
  44. Ng, 2015, Genetics of frontotemporal dementia in Asia: advancing knowledge through collaboration, Neurology, 85, 2060, 10.1212/WNL.0000000000002045 · DOI
  45. Boeve, 2008, Refining frontotemporal dementia with parkinsonism linked to chromosome 17: introducing FTDP-17 (MAPT) and FTDP-17 (PGRN), Arch Neurol., 65, 460, 10.1001/archneur.65.4.460 · DOI
  46. Ghetti, 2015, Invited review: frontotemporal dementia caused by microtubule-associated protein tau gene (MAPT) mutations: a chameleon for neuropathology and neuroimaging, Neuropathol Appl Neurobiol., 41, 24, 10.1111/nan.12213 · DOI
  47. Whitwell, 2009, Atrophy patterns in IVS10+16, IVS10+3, N279K, S305N, P301L, and V337M MAPT mutations, Neurology, 73, 1058, 10.1212/WNL.0b013e3181b9c8b9 · DOI
  48. Renton, 2011, A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD, Neuron, 72, 257, 10.1016/j.neuron.2011.09.010 · DOI · Paper page
  49. Loy, 2014, Genetics of dementia, Lancet, 383, 828, 10.1016/S0140-6736(13)60630-3 · DOI · Paper page
  50. Snowden, 2012, Distinct clinical and pathological characteristics of frontotemporal dementia associated with C9ORF72 mutations, Brain, 135, 693, 10.1093/brain/awr355 · DOI · Paper page
  51. Floeter, 2018, Biomarkers for amyotrophic lateral sclerosis and frontotemporal dementia associated with hexanucleotide expansion mutations in C9orf72, Front Neurol., 9, 1063, 10.3389/fneur.2018.01063 · DOI
  52. Irwin, 2013, Cognitive decline and reduced survival in C9orf72 expansion frontotemporal degeneration and amyotrophic lateral sclerosis, J Neurol Neurosurg Psychiatry, 84, 163, 10.1136/jnnp-2012-303507 · DOI
  53. Toh, 2011, Structure, function, and mechanism of progranulin; the brain and beyond, J Mol Neurosci., 45, 538, 10.1007/s12031-011-9569-4 · DOI
  54. Shankaran, 2008, Missense mutations in the progranulin gene linked to frontotemporal lobar degeneration with ubiquitin-immunoreactive inclusions reduce progranulin production and secretion, J Biol Chem., 283, 1744, 10.1074/jbc.M705115200 · DOI
  55. Gass, 2006, Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration, Hum Mol Genet., 15, 2988, 10.1093/hmg/ddl241 · DOI
  56. Mackenzie, 2016, Molecular neuropathology of frontotemporal dementia: insights into disease mechanisms from postmortem studies, J Neurochem., 138, 54, 10.1111/jnc.13588 · DOI
  57. Rohrer, 2010, Distinct profiles of brain atrophy in frontotemporal lobar degeneration caused by progranulin and tau mutations, Neuroimage, 53, 1070, 10.1016/j.neuroimage.2009.12.088 · DOI
  58. McCluskey, 2014, ALS-Plus syndrome: non-pyramidal features in a large ALS cohort, J Neurol Sci., 345, 118, 10.1016/j.jns.2014.07.022 · DOI
  59. Boxer, 2013, The advantages of frontotemporal degeneration drug development (part 2 of frontotemporal degeneration: the next therapeutic frontier), Alzheimers Dement., 9, 189, 10.1016/j.jalz.2012.03.003 · DOI
  60. Irwin, 2012, Comparison of cerebrospinal fluid levels of tau and Abeta 1-42 in Alzheimer disease and frontotemporal degeneration using 2 analytical platforms, Arch Neurol., 69, 1018, 10.1001/archneurol.2012.26 · DOI · Paper page
  61. Kortvelyessy, 2018, CSF biomarkers of neurodegeneration in progressive non-fluent aphasia and other forms of frontotemporal dementia: clues for pathomechanisms?, Front Neurol., 9, 504, 10.3389/fneur.2018.00504 · DOI
  62. Scherling, 2014, Cerebrospinal fluid neurofilament concentration reflects disease severity in frontotemporal degeneration, Ann Neurol., 75, 116, 10.1002/ana.24052 · DOI · Paper page
  63. Danev, 2010, Early noninvasive diagnosis of neurodegenerative diseases, Folia Med., 52, 5, 10.2478/v10153-010-0041-y · DOI
  64. Zerr, 2009, Updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob disease, Brain, 132, 2659, 10.1093/brain/awp191 · DOI
  65. Vitali, 2011, Diffusion-weighted MRI hyperintensity patterns differentiate CJD from other rapid dementias, Neurology, 76, 1711, 10.1212/WNL.0b013e31821a4439 · DOI
  66. Hu, 2013, Reduced CSF p-Tau181 to Tau ratio is a biomarker for FTLD-TDP, Neurology, 81, 1945, 10.1212/01.wnl.0000436625.63650.27 · DOI · Paper page
  67. Borroni, 2009, Pattern of Tau forms in CSF is altered in progressive supranuclear palsy, Neurobiol Aging, 30, 34, 10.1016/j.neurobiolaging.2007.05.009 · DOI
  68. Teunissen, 2016, Novel diagnostic cerebrospinal fluid biomarkers for pathologic subtypes of frontotemporal dementia identified by proteomics, Alzheimers Dement., 2, 86, 10.1016/j.dadm.2015.12.004 · DOI · Paper page
  69. Brendel, 2018, Comparison of F-T807 and F-THK5117 PET in a mouse model of tau pathology, Front Aging Neurosci., 10, 174, 10.3389/fnagi.2018.00174 · DOI
  70. Goedert, 2018, Tau Filaments and the development of positron emission tomography Tracers, Front Neurol., 9, 70, 10.3389/fneur.2018.00070 · DOI
  71. Lee, 2014, Altered network connectivity in frontotemporal dementia with C9orf72 hexanucleotide repeat expansion, Brain, 137, 3047, 10.1093/brain/awu248 · DOI
  72. McMillan, 2014, Genetic and neuroanatomic associations in sporadic frontotemporal lobar degeneration, Neurobiol Aging, 35, 1473, 10.1016/j.neurobiolaging.2013.11.029 · DOI
  73. Irwin, 2014, Myelin oligodendrocyte basic protein and prognosis in behavioral-variant frontotemporal dementia, Neurology, 83, 502, 10.1212/WNL.0000000000000668 · DOI
  74. Herrmann, 2012, Serotonergic function and treatment of behavioral and psychological symptoms of frontotemporal dementia, Am J Geriatr Psychiatry, 20, 789, 10.1097/JGP.0b013e31823033f3 · DOI
  75. Tsai, 2016, Therapy and clinical trials in frontotemporal dementia: past, present, and future, J Neurochem., 138, 211, 10.1111/jnc.13640 · DOI
  76. Landqvist Waldo, 2013, Frontotemporal dementia with a C9ORF72 expansion in a Swedish family: clinical and neuropathological characteristics, Am J Neurodegener Dis., 2, 276
  77. Steinberg, 2012, Atypical antipsychotic use in patients with dementia: managing safety concerns, Am J Psychiatry, 169, 900, 10.1176/appi.ajp.2012.12030342 · DOI
  78. Chow, 2005, Treatment approaches to symptoms associated with frontotemporal degeneration, Curr Psychiatry Rep., 7, 376, 10.1007/s11920-005-0040-5 · DOI
  79. Vercelletto, 2011, Memantine in behavioral variant frontotemporal dementia: negative results, J Alzheimers Dis., 23, 749, 10.3233/JAD-2010-101632 · DOI
  80. Mocellin, 2015, Clinical update on frontotemporal dementia: diagnosis and treatment, Australas Psychiatry, 23, 481, 10.1177/1039856215582276 · DOI
  81. Sanders, 2014, Distinct tau prion strains propagate in cells and mice and define different tauopathies, Neuron, 82, 1271, 10.1016/j.neuron.2014.04.047 · DOI · Paper page
  82. Yanamandra, 2013, Anti-tau antibodies that block tau aggregate seeding in vitro markedly decrease pathology and improve cognition in vivo, Neuron, 80, 402, 10.1016/j.neuron.2013.07.046 · DOI · Paper page
  83. Wischik, 2014, Tau-aggregation inhibitor therapy for Alzheimer's disease, Biochem Pharmacol., 88, 529, 10.1016/j.bcp.2013.12.008 · DOI
  84. Coughlin, 2017, Emerging diagnostic and therapeutic strategies for tauopathies, Curr Neurol Neurosci Rep., 17, 72, 10.1007/s11910-017-0779-1 · DOI
  85. Mancini, 2018, Phenylindanes in brewed coffee inhibit amyloid-beta and tau aggregation, Front Neurosci., 12, 735, 10.3389/fnins.2018.00735 · DOI
  86. Buchholz, 2008, Interactions of methylene blue with human disulfide reductases and their orthologues from Plasmodium falciparum, Antimicrob Agents Chemother., 52, 183, 10.1128/AAC.00773-07 · DOI
  87. Heard, 2018, Repurposing proteostasis-modifying drugs to prevent or treat age-related dementia: a systematic review, Front Physiol., 9, 1520, 10.3389/fphys.2018.01520 · DOI
  88. Wischik, 1996, Selective inhibition of Alzheimer disease-like tau aggregation by phenothiazines, Proc Natl Acad Sci USA., 93, 11213, 10.1073/pnas.93.20.11213 · DOI · Paper page
  89. Matsuoka, 2008, A neuronal microtubule-interacting agent, NAPVSIPQ, reduces tau pathology and enhances cognitive function in a mouse model of Alzheimer's disease, J Pharmacol Exp Ther., 325, 146, 10.1124/jpet.107.130526 · DOI
  90. Pedersen, 2015, Tau immunotherapy for Alzheimer's disease, Trends Mol Med., 21, 394, 10.1016/j.molmed.2015.03.003 · DOI · Paper page
  91. Medina, 2014, New insights into the role of glycogen synthase kinase-3 in Alzheimer's disease, Expert Opin Ther Targets, 18, 69, 10.1517/14728222.2013.843670 · DOI
  92. West, 2017, Preclinical and clinical development of ABBV-8E12, a humanized anti-tau antibody, for treatment of Alzheimer's disease and other tauopathies, J Prev Alzheimers Dis., 4, 236, 10.14283/jpad.2017.36 · DOI
  93. Panza, 2016, Tau-centric targets and drugs in clinical development for the treatment of Alzheimer's disease, Biomed Res Int., 2016, 3245935, 10.1155/2016/3245935 · DOI · Paper page
  94. O'Brien, 2017, Clinical practice with anti-dementia drugs: a revised (third) consensus statement from the British Association for Psychopharmacology, J Psychopharmacol., 31, 147, 10.1177/0269881116680924 · DOI
  95. Lagier-Tourenne, 2013, Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration, Proc Natl Acad Sci USA., 110, E4530, 10.1073/pnas.1318835110 · DOI
  96. Kramer, 2016, Spt4 selectively regulates the expression of C9orf72 sense and antisense mutant transcripts, Science, 353, 708, 10.1126/science.aaf7791 · DOI
  97. DeVos, 2013, Antisense reduction of tau in adult mice protects against seizures, J Neurosci., 33, 12887, 10.1523/JNEUROSCI.2107-13.2013 · DOI · Paper page
  98. Cenik, 2011, Suberoylanilide hydroxamic acid (vorinostat) up-regulates progranulin transcription: rational therapeutic approach to frontotemporal dementia, J Biol Chem., 286, 16101, 10.1074/jbc.M110.193433 · DOI
  99. Capell, 2011, Rescue of progranulin deficiency associated with frontotemporal lobar degeneration by alkalizing reagents and inhibition of vacuolar ATPase, J Neurosci., 31, 1885, 10.1523/JNEUROSCI.5757-10.2011 · DOI
  100. Whitwell, 2012, Neuroimaging signatures of frontotemporal dementia genetics: C9ORF72, tau, progranulin and sporadics, Brain, 135, 794, 10.1093/brain/aws001 · DOI · Paper page
  101. Alberici, 2014, Results from a pilot study on amiodarone administration in monogenic frontotemporal dementia with granulin mutation, Neurol Sci., 35, 1215, 10.1007/s10072-014-1683-y · DOI

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Metadata

Authors
Liu, M.-N., Lau, C.-I., & Lin, C.-P.
Venue
Frontiers in Psychiatry
Publisher
Frontiers Media SA
Published
2019-02-21
Volume
10
ISSN
1664-0640
DOI
10.3389/fpsyt.2019.00075
PMC
PMC6393374
Cited by
20
References
15
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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