| Sonstiges: |
- Nachgewiesen in: MEDLINE
- Sprachen: English
- Publication Type: Journal Article; Review; Research Support, Non-U.S. Gov't
- Language: English
- [Nat Rev Neurol] 2024 Jun; Vol. 20 (6), pp. 337-346. <i>Date of Electronic Publication: </i>2024 May 09.
- MeSH Terms: Biomarkers* / metabolism ; Humans ; Alzheimer Disease / physiopathology ; Alzheimer Disease / diagnosis ; Alzheimer Disease / metabolism ; tau Proteins / metabolism ; Neurodegenerative Diseases / physiopathology ; Neurodegenerative Diseases / diagnosis ; Cognitive Dysfunction / physiopathology ; Cognitive Dysfunction / diagnosis ; Cognitive Dysfunction / etiology ; Clinical Relevance
- References: Glenner, G. G. & Wong, C. W. Alzheimer’s disease and Down’s syndrome: sharing of a unique cerebrovascular amyloid fibril protein. Biochem. Biophys. Res. Commun. 122, 1131–1135 (1984). (PMID: 623680510.1016/0006-291X(84)91209-9) ; Hardy, J. & Selkoe, D. J. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 297, 353–356 (2002). (PMID: 1213077310.1126/science.1072994) ; Jack, C. R. Jr et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 7, 257–262 (2011). (PMID: 2151424710.1016/j.jalz.2011.03.004) ; Jack, C. R. Jr et al. An operational approach to National Institute on Aging-Alzheimer’s Association criteria for preclinical Alzheimer disease. Ann. Neurol. 71, 765–775 (2012). (PMID: 22488240358622310.1002/ana.22628) ; Sperling, R. A. et al. Toward defining the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Assocation workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 7, 280–292 (2011). (PMID: 2151424810.1016/j.jalz.2011.03.003) ; Jack, C. R. Jr et al. Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurol. 9, 119–128 (2010). (PMID: 20083042281984010.1016/S1474-4422(09)70299-6) ; Power, M. C. et al. Combined neuropathological pathways account for age-related risk of dementia. Ann. Neurol. 84, 10–22 (2018). (PMID: 29944741611951810.1002/ana.25246) ; Kawas, C. H. et al. Multiple pathologies are common and related to dementia in the oldest-old: the 90+ study. Neurology 85, 535–542 (2015). (PMID: 26180144454024610.1212/WNL.0000000000001831) ; Knopman, D. S. et al. Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease. Neurology 78, 1576–1582 (2012). (PMID: 22551733334884810.1212/WNL.0b013e3182563bbe) ; Blennow, K. Cerebrospinal fluid protein biomarkers for Alzheimer’s disease. NeuroRx 1, 213–225 (2004). (PMID: 1571702253492910.1602/neurorx.1.2.213) ; Hansson, O. et al. CSF biomarkers of Alzheimer’s disease concord with amyloid-β PET and predict clinical progression: a study of fully automated immunoassays in BioFINDER and ADNI cohorts. Alzheimers Dement. 14, 1470–1481 (2018). (PMID: 2949917110.1016/j.jalz.2018.01.010) ; Klunk, W. E. et al. Imaging brain amyloid in Alzheimer’s disease with Pittsburgh Compound-B. Ann. Neurol. 55, 306–319 (2004). (PMID: 1499180810.1002/ana.20009) ; Schwarz, C. G. et al. Considerations for performing level-2 Centiloid transformations for amyloid PET SUVR values. Sci. Rep. 8, 7421 (2018). (PMID: 29743601594352110.1038/s41598-018-25459-9) ; Chien, D. T. et al. Early clinical PET imaging results with the novel PHF-tau radioligand [F-18]-T807. J. Alzheimers Dis. 34, 457–468 (2013). (PMID: 2323487910.3233/JAD-122059) ; Jack, C. R. Jr et al. A/T/N: an unbiased descriptive classification scheme for Alzheimer disease biomarkers. Neurology 87, 539–547 (2016). (PMID: 27371494497066410.1212/WNL.0000000000002923) ; Jack, C. R. et al. Age-specific and sex-specific prevalence of cerebral β-amyloidosis, tauopathy, and neurodegeneration in cognitively unimpaired individuals aged 50-95 years: a cross-sectional study. Lancet Neurol. 16, 435–444 (2017). (PMID: 28456479551653410.1016/S1474-4422(17)30077-7) ; Jack, C. R. Jr et al. Suspected non-Alzheimer disease pathophysiology – concept and controversy. Nat. Rev. Neurol. 12, 117–124 (2016). (PMID: 26782335478425710.1038/nrneurol.2015.251) ; Dodich, A. et al. The A/T/N model applied through imaging biomarkers in a memory clinic. Eur. J. Nucl. Med. Mol. Imaging 47, 247–255 (2020). (PMID: 3179257310.1007/s00259-019-04536-9) ; Ebenau, J. L. et al. ATN classification and clinical progression in subjective cognitive decline: the SCIENCe project. Neurology 95, e46–e58 (2020). (PMID: 32522798737137610.1212/WNL.0000000000009724) ; Ingala, S. et al. Application of the ATN classification scheme in a population without dementia: findings from the EPAD cohort. Alzheimers Dement. 17, 1189–1204 (2021). (PMID: 3381174210.1002/alz.12292) ; Ekman, U., Ferreira, D. & Westman, E. The A/T/N biomarker scheme and patterns of brain atrophy assessed in mild cognitive impairment. Sci. Rep. 8, 8431 (2018). (PMID: 29849029597671310.1038/s41598-018-26151-8) ; Delmotte, K., Schaeverbeke, J., Poesen, K. & Vandenberghe, R. Prognostic value of amyloid/tau/neurodegeneration (ATN) classification based on diagnostic cerebrospinal fluid samples for Alzheimer’s disease. Alzheimers Res. Ther. 13, 84 (2021). (PMID: 33879243805919710.1186/s13195-021-00817-4) ; Janelidze, S. et al. Cerebrospinal fluid p-tau217 performs better than p-tau181 as a biomarker of Alzheimer’s disease. Nat. Commun. 11, 1683 (2020). (PMID: 32246036712521810.1038/s41467-020-15436-0) ; Barthelemy, N. R. et al. Cerebrospinal fluid phospho-tau T217 outperforms T181 as a biomarker for the differential diagnosis of Alzheimer’s disease and PET amyloid-positive patient identification. Alzheimers Res. Ther. 12, 26 (2020). (PMID: 32183883707945310.1186/s13195-020-00596-4) ; Soldan, A. et al. ATN profiles among cognitively normal individuals and longitudinal cognitive outcomes. Neurology 92, E1567–E1579 (2019). (PMID: 30842300644844910.1212/WNL.0000000000007248) ; Gordon, B. A. et al. Longitudinal β-amyloid deposition and hippocampal volume in preclinical Alzheimer disease and suspected non-Alzheimer disease pathophysiology. JAMA Neurol. 73, 1192–1200 (2016). (PMID: 27548756523738110.1001/jamaneurol.2016.2642) ; Vos, S. J. et al. Prevalence and prognosis of Alzheimer’s disease at the mild cognitive impairment stage. Brain 138, 1327–1338 (2015). (PMID: 25693589501393010.1093/brain/awv029) ; Chung, J. K. et al. The effects of cortical hypometabolism and hippocampal atrophy on clinical trajectories in mild cognitive impairment with suspected non-Alzheimer’s pathology: a brief report. J. Alzheimers Dis. 60, 341–347 (2017). (PMID: 2882617810.3233/JAD-170098) ; Wisse, L. E. M. et al. Suspected non-AD pathology in mild cognitive impairment. Neurobiol. Aging 36, 3152–3162 (2015). (PMID: 26422359464177410.1016/j.neurobiolaging.2015.08.029) ; Altomare, D. et al. Applying the ATN scheme in a memory clinic population: the ABIDE project. Neurology 93, e1635–e1646 (2019). (PMID: 3159771010.1212/WNL.0000000000008361) ; Vos, S. J. B. et al. NIA-AA staging of preclinical Alzheimer disease: discordance and concordance of CSF and imaging biomarkers. Neurobiol. Aging 44, 1–8 (2016). (PMID: 27318129491303910.1016/j.neurobiolaging.2016.03.025) ; Baldeiras, I. et al. Addition of the Aβ42/40 ratio to the cerebrospinal fluid biomarker profile increases the predictive value for underlying Alzheimer’s disease dementia in mild cognitive impairment. Alzheimers Res. Ther. 10, 33 (2018). (PMID: 29558986586163410.1186/s13195-018-0362-2) ; Soldan, A. et al. Hypothetical preclinical Alzheimer disease groups and longitudinal cognitive change. JAMA Neurol. 73, 698–705 (2016). (PMID: 27064267517332710.1001/jamaneurol.2016.0194) ; Toledo, J. B. et al. Neuronal injury biomarkers and prognosis in ADNI subjects with normal cognition. Acta Neuropathol. Commun. 2, 26 (2014). (PMID: 24602322400825810.1186/2051-5960-2-26) ; Burnham, S. C. et al. Clinical and cognitive trajectories in cognitively healthy elderly individuals with suspected non-Alzheimer’s disease pathophysiology (SNAP) or Alzheimer’s disease pathology: a longitudinal study. Lancet Neurol. 15, 1044–1053 (2016). (PMID: 2745047110.1016/S1474-4422(16)30125-9) ; Bos, I. et al. Vascular risk factors are associated with longitudinal changes in cerebrospinal fluid tau markers and cognition in preclinical Alzheimer’s disease. Alzheimers Dement. 15, 1149–1159 (2019). (PMID: 3137857510.1016/j.jalz.2019.04.015) ; Calvin, C. M. et al. Prediction of Alzheimer’s disease biomarker status defined by the ‘ATN framework’ among cognitively healthy individuals: results from the EPAD longitudinal cohort study. Alzheimers Res. Ther. 12, 143 (2020). (PMID: 33168064765016910.1186/s13195-020-00711-5) ; Knopman, D. S. et al. Brain injury biomarkers are not dependent on β-amyloid in normal elderly. Ann. Neurol. 73, 472–480 (2013). (PMID: 23424032366040810.1002/ana.23816) ; Delvenne, A. et al. Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non-Alzheimer’s disease pathophysiology. Alzheimers Dement. 19, 807–820 (2023). (PMID: 10.1002/alz.12713) ; Alcolea, D. et al. Amyloid precursor protein metabolism and inflammation markers in preclinical Alzheimer disease. Neurology 85, 626–633 (2015). (PMID: 2618013910.1212/WNL.0000000000001859) ; Hohman, T. J. et al. APOE allele frequencies in suspected non-amyloid pathophysiology (SNAP) and the prodromal stages of Alzheimer’s disease. PLoS ONE 12, e0188501 (2017). (PMID: 29190651570877710.1371/journal.pone.0188501) ; Schreiber, S. et al. Alzheimer disease signature neurodegeneration and APOE genotype in mild cognitive impairment with suspected non-Alzheimer disease pathophysiology. JAMA Neurol. 74, 650–659 (2017). (PMID: 28319241582221010.1001/jamaneurol.2016.5349) ; Thal, D. R. et al. Estimation of amyloid distribution by [ 18 F]flutemetamol PET predicts the neuropathological phase of amyloid β-protein deposition. Acta Neuropathol. 136, 557–567 (2018). (PMID: 30123935613294410.1007/s00401-018-1897-9) ; La Joie, R. et al. Multisite study of the relationships between antemortem [ 11 C]PIB-PET Centiloid values and postmortem measures of Alzheimer’s disease neuropathology. Alzheimers Dement. 15, 205–216 (2019). (PMID: 3034718810.1016/j.jalz.2018.09.001) ; Nakamura, A. et al. High performance plasma amyloid-β biomarkers for Alzheimer’s disease. Nature 554, 249–254 (2018). (PMID: 2942047210.1038/nature25456) ; Willemse, E. A. J. et al. Comparing CSF amyloid-β biomarker ratios for two automated immunoassays, Elecsys and Lumipulse, with amyloid PET status. Alzheimers Dement. 13, e12182 (2021). ; Lowe, V. J. et al. Neuroimaging correlates with neuropathologic schemes in neurodegenerative disease. Alzheimers Dement. 15, 927–939 (2019). (PMID: 3117502510.1016/j.jalz.2019.03.016) ; Vos, S. J. et al. Preclinical Alzheimer’s disease and its outcome: a longitudinal cohort study. Lancet Neurol. 12, 957–965 (2013). (PMID: 24012374390467810.1016/S1474-4422(13)70194-7) ; Wisse, L. E. M. et al. Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology. Alzheimers Res. Ther. 13, 100 (2021). (PMID: 33990226812254910.1186/s13195-021-00835-2) ; Thal, D. R., Rub, U., Orantes, M. & Braak, H. Phases of Aβ-deposition in the human brain and its relevance for the development of AD. Neurology 58, 1791–1800 (2002). (PMID: 1208487910.1212/WNL.58.12.1791) ; Crary, J. F. et al. Primary age-related tauopathy (PART): a common pathology associated with human aging. Acta Neuropathol. 128, 755–766 (2014). (PMID: 25348064425784210.1007/s00401-014-1349-0) ; Duyckaerts, C. et al. PART is part of Alzheimer disease. Acta Neuropathol. 129, 749–756 (2015). (PMID: 25628035440534910.1007/s00401-015-1390-7) ; Thal, D. R. & Tome, S. O. The central role of tau in Alzheimer’s disease: from neurofibrillary tangle maturation to the induction of cell death. Brain Res. Bull. 190, 204–217 (2022). (PMID: 3624458110.1016/j.brainresbull.2022.10.006) ; Walkiewicz, G. et al. Primary retinal tauopathy: a tauopathy with a distinct molecular pattern. Alzheimers Dement. 20, 330–340 (2024). (PMID: 3761527510.1002/alz.13424) ; Shi, Y. et al. Cryo-EM structures of tau filaments from Alzheimer’s disease with PET ligand APN-1607. Acta Neuropathol. 141, 697–708 (2021). (PMID: 33723967804386410.1007/s00401-021-02294-3) ; Kaufman, S. K., Del Tredici, K., Thomas, T. L., Braak, H. & Diamond, M. I. Tau seeding activity begins in the transentorhinal/entorhinal regions and anticipates phospho-tau pathology in Alzheimer’s disease and PART. Acta Neuropathol. 136, 57–67 (2018). (PMID: 29752551601509810.1007/s00401-018-1855-6) ; Aragao Gomes, L. et al. Maturation of neuronal AD-tau pathology involves site-specific phosphorylation of cytoplasmic and synaptic tau preceding conformational change and fibril formation. Acta Neuropathol. 141, 173–192 (2021). (PMID: 3342793810.1007/s00401-020-02251-6) ; Braak, H., Thal, D. R., Ghebremedhin, E. & Del Tredici, K. Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years. J. Neuropathol. Exp. Neurol. 70, 960–969 (2011). (PMID: 2200242210.1097/NEN.0b013e318232a379) ; Santa-Maria, I. et al. The MAPT H1 haplotype is associated with tangle-predominant dementia. Acta Neuropathol. 124, 693–704 (2012). (PMID: 22802095360847510.1007/s00401-012-1017-1) ; Farrell, K. et al. Genome-wide association study and functional validation implicates JADE1 in tauopathy. Acta Neuropathol. 143, 33–53 (2022). (PMID: 3471976510.1007/s00401-021-02379-z) ; Teylan, M. et al. Clinical diagnoses among individuals with primary age-related tauopathy versus Alzheimer’s neuropathology. Lab. Invest. 99, 1049–1055 (2019). (PMID: 30710118660947810.1038/s41374-019-0186-0) ; Glenner, G. G. & Wong, C. W. Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem. Biophys. Res. Commun. 120, 885–890 (1984). (PMID: 637566210.1016/S0006-291X(84)80190-4) ; Thal, D. R., Ghebremedhin, E., Orantes, M. & Wiestler, O. D. Vascular pathology in Alzheimer disease: correlation of cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis with cognitive decline. J. Neuropathol. Exp. Neurol. 62, 1287–1301 (2003). (PMID: 1469270410.1093/jnen/62.12.1287) ; Thal, D. R. et al. Pathology of clinical and preclinical Alzheimer’s disease. Eur. Arch. Psychiatry Clin. Neurosci. 263, S137–S145 (2013). (PMID: 2407789010.1007/s00406-013-0449-5) ; Charidimou, A. et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy: a multicentre, retrospective, MRI-neuropathology diagnostic accuracy study. Lancet Neurol. 21, 714–725 (2022). (PMID: 35841910938945210.1016/S1474-4422(22)00208-3) ; Boyle, P. A. et al. Cerebral amyloid angiopathy and cognitive outcomes in community-based older persons. Neurology 85, 1930–1936 (2015). (PMID: 26537052466412510.1212/WNL.0000000000002175) ; Hyman, B. T. et al. National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease. Alzheimers Dement. 8, 1–13 (2012). (PMID: 2226558710.1016/j.jalz.2011.10.007) ; Ellis, R. J. et al. Cerebral amyloid angiopathy in the brains of patients with Alzheimer’s disease: the CERAD experience, Part XV. Neurology 46, 1592–1596 (1996). (PMID: 864955410.1212/WNL.46.6.1592) ; Selnes, O. A. & Vinters, H. V. Vascular cognitive impairment. Nat. Clin. Pract. Neurol. 2, 538–547 (2006). (PMID: 1699082710.1038/ncpneuro0294) ; Thal, D. R. et al. Capillary cerebral amyloid angiopathy is associated with vessel occlusion and cerebral blood flow disturbances. Neurobiol. Aging 30, 1936–1948 (2009). (PMID: 1835913110.1016/j.neurobiolaging.2008.01.017) ; Hecht, M., Kramer, L. M., von Arnim, C. A. F., Otto, M. & Thal, D. R. Capillary cerebral amyloid angiopathy in Alzheimer’s disease: association with allocortical/hippocampal microinfarcts and cognitive decline. Acta Neuropathol. 135, 681–694 (2018). (PMID: 2957459110.1007/s00401-018-1834-y) ; Gorelick, P. B. et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42, 2672–2713 (2011). (PMID: 21778438377866910.1161/STR.0b013e3182299496) ; Skrobot, O. A. et al. Vascular cognitive impairment neuropathology guidelines (VCING): the contribution of cerebrovascular pathology to cognitive impairment. Brain 139, 2957–2969 (2016). (PMID: 2759111310.1093/brain/aww214) ; Vinters, H. V. et al. Neuropathologic substrates of ischemic vascular dementia. J. Neuropathol. Exp. Neurol. 59, 931–945 (2000). (PMID: 1108957110.1093/jnen/59.11.931) ; Launer, L. J., Hughes, T. M. & White, L. R. Microinfarcts, brain atrophy, and cognitive function: the Honolulu Asia Aging Study Autopsy Study. Ann. Neurol. 70, 774–780 (2011). (PMID: 22162060324100510.1002/ana.22520) ; Thal, D. R. et al. Stages of granulovacuolar degeneration: their relation to Alzheimer’s disease and chronic stress response. Acta Neuropathol. 122, 577–589 (2011). (PMID: 2193563710.1007/s00401-011-0871-6) ; Simchowicz, T. in Histologie und histopathologische Arbeiten über die Großhirnrinde mit besonderer Berücksichtigung der pathologischen Anatomie der Geistekrankheiten Vol. 4 (eds Nissl, F. & Alzheimer, A.) 267–444 (Fischer, 1911). ; Ball, M. J. & Lo, P. Granulovacuolar degeneration in the ageing brain and in dementia. J. Neuropathol. Exp. Neurol. 36, 474–487 (1977). (PMID: 87062210.1097/00005072-197705000-00006) ; Funk, K. E., Mrak, R. E. & Kuret, J. Granulovacuolar degeneration (GVD) bodies of Alzheimer’s disease (AD) resemble late-stage autophagic organelles. Neuropathol. Appl. Neurobiol. 37, 295–306 (2011). (PMID: 20946470303797610.1111/j.1365-2990.2010.01135.x) ; Kohler, C. Granulovacuolar degeneration: a neurodegenerative change that accompanies tau pathology. Acta Neuropathol. 132, 339–359 (2016). (PMID: 2706226010.1007/s00401-016-1562-0) ; Koper, M. J. et al. Necrosome complex detected in granulovacuolar degeneration is associated with neuronal loss in Alzheimer’s disease. Acta Neuropathol. 139, 463–484 (2020). (PMID: 3180223710.1007/s00401-019-02103-y) ; Wiersma, V. I. et al. Granulovacuolar degeneration bodies are neuron-selective lysosomal structures induced by intracellular tau pathology. Acta Neuropathol. 138, 943–970 (2019). (PMID: 31456031685149910.1007/s00401-019-02046-4) ; Balusu, S. et al. MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer’s disease. Science 381, 1176–1182 (2023). (PMID: 37708272761523610.1126/science.abp9556) ; Tang, D., Kang, R., Berghe, T. V., Vandenabeele, P. & Kroemer, G. The molecular machinery of regulated cell death. Cell Res. 29, 347–364 (2019). (PMID: 30948788679684510.1038/s41422-019-0164-5) ; Koper, M. J. et al. LATE-NC aggravates GVD-mediated necroptosis in Alzheimer’s disease. Acta Neuropathol. Commun. 10, 128 (2022). (PMID: 36057624944110010.1186/s40478-022-01432-6) ; Josephs, K. A. et al. Updated TDP-43 in Alzheimer’s disease staging scheme. Acta Neuropathol. 131, 571–585 (2016). (PMID: 26810071594669210.1007/s00401-016-1537-1) ; Joachim, C. L., Morris, J. H. & Selkoe, D. J. Clinically diagnosed Alzheimer’s disease: autopsy results in 150 cases. Ann. Neurol. 24, 50–56 (1988). (PMID: 341520010.1002/ana.410240110) ; Nelson, P. T. et al. Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report. Brain 142, 1503–1527 (2019). (PMID: 31039256653684910.1093/brain/awz099) ; Nelson, P. T. et al. LATE-NC staging in routine neuropathologic diagnosis: an update. Acta Neuropathol. 145, 159–173 (2023). (PMID: 3651206110.1007/s00401-022-02524-2) ; Amador-Ortiz, C. et al. TDP-43 immunoreactivity in hippocampal sclerosis and Alzheimer’s disease. Ann. Neurol. 61, 435–445 (2007). (PMID: 17469117267720410.1002/ana.21154) ; Tome, S. O. et al. TDP-43 pathology is associated with increased tau burdens and seeding. Mol. Neurodegener. 18, 71 (2023). (PMID: 377778061054419210.1186/s13024-023-00653-0) ; Braun, D. J. et al. Early chronic suppression of microglial p38ɑ in a model of Alzheimer’s disease does not significantly alter amyloid-associated neuropathology. PLoS ONE 18, e0286495 (2023). (PMID: 372568811023177310.1371/journal.pone.0286495) ; McAleese, K. E. et al. TDP-43 pathology in Alzheimer’s disease, dementia with Lewy bodies and ageing. Brain Pathol. 27, 472–479 (2017). (PMID: 2749526710.1111/bpa.12424) ; Mackenzie, I. R. et al. Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration: an update. Acta Neuropathol. 119, 1–4 (2010). (PMID: 1992442410.1007/s00401-009-0612-2) ; Braak, H. & Braak, E. Argyrophilic grain disease: frequency of occurrence in different age categories and neuropathological diagnostic criteria. J. Neural Transm. 105, 801–819 (1998). (PMID: 986932010.1007/s007020050096) ; Thal, D. R. et al. The impact of argyrophilic grain disease on the development of dementia and its relationship to concurrent Alzheimer’s disease-related pathology. Neuropathol. Appl. Neurobiol. 31, 270–279 (2005). (PMID: 1588506410.1111/j.1365-2990.2005.00635.x) ; Thal, D. R. et al. Frontotemporal lobar degeneration FTLD-tau: preclinical lesions, vascular, and Alzheimer-related co-pathologies. J. Neural Transm. 122, 1007–1018 (2015). (PMID: 2555695010.1007/s00702-014-1360-6) ; Josephs, K. A. et al. Argyrophilic grains: a distinct disease or an additive pathology? Neurobiol. Aging 29, 566–573 (2008). (PMID: 1718878310.1016/j.neurobiolaging.2006.10.032) ; Braak, H. et al. Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol. Aging 24, 197–211 (2003). (PMID: 1249895410.1016/S0197-4580(02)00065-9) ; Del Tredici, K., Rub, U., De Vos, R. A., Bohl, J. R. & Braak, H. Where does Parkinson disease pathology begin in the brain? J. Neuropathol. Exp. Neurol. 61, 413–426 (2002). (PMID: 1203026010.1093/jnen/61.5.413) ; Brettschneider, J. et al. Stages of pTDP-43 pathology in amyotrophic lateral sclerosis. Ann. Neurol. 74, 20–38 (2013). (PMID: 23686809378507610.1002/ana.23937) ; Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006). (PMID: 1702365910.1126/science.1134108) ; Van Schoor, E. et al. Necrosome-positive granulovacuolar degeneration is associated with TDP-43 pathological lesions in the hippocampus of ALS/FTLD cases. Neuropathol. Appl. Neurobiol. 47, 328–345 (2020). (PMID: 3294904710.1111/nan.12668) ; Fernandes Gomes, B. et al. ɑ-Synuclein seed amplification assay as a diagnostic tool for parkinsonian disorders. Parkinsonism Relat. Disord. 117, 105807 (2023). (PMID: 3759170910.1016/j.parkreldis.2023.105807) ; Shen, X. N. et al. Plasma amyloid, tau, and neurodegeneration biomarker profiles predict Alzheimer’s disease pathology and clinical progression in older adults without dementia. Alzheimers Dement. 12, e12104 (2020). ; Cummings, J. et al. Alzheimer’s disease drug development pipeline: 2023. Alzheimers Dement. 9, e12385 (2023). (PMID: 10.1002/trc2.12385) ; Nelson, P. T. et al. Frequency of LATE neuropathologic change across the spectrum of Alzheimer’s disease neuropathology: combined data from 13 community-based or population-based autopsy cohorts. Acta Neuropathol. 144, 27–44 (2022). (PMID: 35697880955293810.1007/s00401-022-02444-1) ; Hamilton, R. L. Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using ɑ-synuclein immunohistochemistry. Brain Pathol. 10, 378–384 (2000). (PMID: 1088565610.1111/j.1750-3639.2000.tb00269.x) ; Lippa, C. F. et al. Lewy bodies contain altered α-synuclein in brains of many familial Alzheimer’s disease patients with mutations in presenilin and amyloid precursor protein genes. Am. J. Pathol. 153, 1365–1370 (1998). (PMID: 9811326185339110.1016/S0002-9440(10)65722-7) ; Uchikado, H., Lin, W. L., DeLucia, M. W. & Dickson, D. W. Alzheimer disease with amygdala Lewy bodies: a distinct form of α-synucleinopathy. J. Neuropathol. Exp. Neurol. 65, 685–697 (2006). (PMID: 1682595510.1097/01.jnen.0000225908.90052.07) ; Vonsattel, J. P. et al. Cerebral amyloid angiopathy without and with cerebral hemorrhages: a comparative histological study. Ann. Neurol. 30, 637–649 (1991). (PMID: 176389010.1002/ana.410300503) ; Mandybur, T. I. Cerebral amyloid angiopathy: the vascular pathology and complications. J. Neuropathol. Exp. Neurol. 45, 79–90 (1986). (PMID: 394132810.1097/00005072-198601000-00007) ; Dickson, D. W., Kouri, N., Murray, M. E. & Josephs, K. A. Neuropathology of frontotemporal lobar degeneration-tau (FTLD-tau). J. Mol. Neurosci. 45, 384–389 (2011). (PMID: 21720721320812810.1007/s12031-011-9589-0) ; Jansen, W. J. et al. Prevalence estimates of amyloid abnormality across the Alzheimer disease clinical spectrum. JAMA Neurol. 79, 228–243 (2022). (PMID: 3509950910.1001/jamaneurol.2021.5216) ; Mormino, E. C. et al. Heterogeneity in suspected non-Alzheimer disease pathophysiology among clinically normal older individuals. JAMA Neurol. 73, 1185–1191 (2016). (PMID: 27548655526652210.1001/jamaneurol.2016.2237) ; Murray, M. E. et al. Clinicopathologic and 11 C-Pittsburgh compound B implications of Thal amyloid phase across the Alzheimer’s disease spectrum. Brain 138, 1370–1381 (2015). (PMID: 25805643440719010.1093/brain/awv050) ; Tan, M.-S. et al. Longitudinal trajectories of Alzheimer’s ATN biomarkers in elderly persons without dementia. Alzheimers Res. Ther. 12, 55 (2020). (PMID: 32393375721671410.1186/s13195-020-00621-6)
- Substance Nomenclature: 0 (Biomarkers) ; 0 (tau Proteins)
- Entry Date(s): Date Created: 20240509 Date Completed: 20240604 Latest Revision: 20240613
- Update Code: 20240614
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