Volume 22 Issue 6
Jun.  2024
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GAO Song, ZHANG Min, LU Yuan. Research progress on biomarkers of mild cognitive impairment[J]. Chinese Journal of General Practice, 2024, 22(6): 1043-1046. doi: 10.16766/j.cnki.issn.1674-4152.003562
Citation: GAO Song, ZHANG Min, LU Yuan. Research progress on biomarkers of mild cognitive impairment[J]. Chinese Journal of General Practice, 2024, 22(6): 1043-1046. doi: 10.16766/j.cnki.issn.1674-4152.003562

Research progress on biomarkers of mild cognitive impairment

doi: 10.16766/j.cnki.issn.1674-4152.003562
Funds:

 201940495

 PWYq2020-03

  • Received Date: 2023-06-25
    Available Online: 2024-07-22
  • Mild cognitive impairment (MCI) is a clinical transitional state between normal aging and dementia, which is considered to be the preclinical stage of Alzheimer's disease (AD). Due to the irreversible nature of the course of AD, and the lack of clinically available therapies to improve or delay the disease progression, the early detection, diagnosis and intervention of MCI are crucial in reducing the incidence of AD and delaying its progression. On one hand, research on biomarkers can serve as the foundation for elucidating the pathological mechanisms underlying the disease. On the other hand, it provides objective evidence for early screening and diagnosis. This paper reviewed the research progress of MCI biomarkers from the cerebrospinal fluid, blood and genetics perspectives with a focus on the analysis and discussion advancements in biomarkers (especially amyloid protein, phosphorylated tau protein) found in cerebrospinal fluid and blood. The study of biomarkers from different sources and pathways has their own advantages and disadvantages. MCI hematological biomarkers have significant potential for clinical translation with promising research prospects. The standardization of biomarkers is still a major direction in MCI research field.

     

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  • [1]
    PETERSEN R C. Mild cognitive impairment[J]. Continuum (Minneap Minn), 2016, 22(2Dementia): 404-418.
    [2]
    PETERSEN R C. Mild cognitive impairment: transition between aging and Alzheimer's disease[J]. Neurologia, 2000, 15(3): 93-101.
    [3]
    ALBERT M S, DEKOSKY S T, DICKSON D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease[J]. Alzheimers Dement, 2011, 7(3): 270-279. doi: 10.1016/j.jalz.2011.03.008
    [4]
    CLIFFORD R J, DAVID A B, KAJ B, et al. NIA-AA Research Framework: toward a biological definition of Alzheimer's disease[J]. Alzheimers Dement, 2018, 14(4): 535-562. doi: 10.1016/j.jalz.2018.02.018
    [5]
    ZETTERBERG H, PEDERSEN M, LIND K, et al. Intra-individual stability of CSF biomarkers for Alzheimer's disease over two years[J]. J Alzheimers Dis, 2007, 12(3): 255-260. doi: 10.3233/JAD-2007-12307
    [6]
    BUCHHAVE P, MINTHON L, ZETTERBERG H, et al. Cerebrospinal fluid levels of beta-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia[J]. Arch Gen Psychiatry, 2012, 69(1): 98-106. doi: 10.1001/archgenpsychiatry.2011.155
    [7]
    STENH C, ENGLUND H, LORD A, et al. Amyloid-beta oligomers are inefficiently measured by enzyme-linked immunosorbent assay[J]. Ann Neurol, 2005, 58(1): 147-150. doi: 10.1002/ana.20524
    [8]
    HANSSON O, ZETTERBERG H, BUCHHAVE P, et al. Prediction of Alzheimer's disease using the CSF Abeta42/Abeta40 ratio in patients with mild cognitive impairment[J]. Dement Geriatr Cogn Disord, 2007, 23(5): 316-320. doi: 10.1159/000100926
    [9]
    MA Y, BRETTSCHNEIDER J, COLLINGWOOD J F. A systematic review and meta-analysis of cerebrospinal fluid amyloid and tau levels identifies mild cognitive impairment patients progressing to Alzheimer's disease[J]. Biomedicines, 2022, 10(7): 1713. DOI: 10.3390/biomedicines10071713.
    [10]
    OLSSON B, LAUTNER R, ANDREASSON U, et al. CSF and blood biomarkers for the diagnosis of Alzheimer's disease: a systematic review and meta-analysis[J]. Lancet Neurol, 2016, 15(7): 673-684. doi: 10.1016/S1474-4422(16)00070-3
    [11]
    HARALD H, KATHARINA B, JENS C P, et al. Correlation of cerebrospinal fluid levels of tau protein phosphorylated at threonine 231 with rates of hippocampal atrophy in Alzheimer's disease[J]. Archives of Neurology, 2005, 62(5): 770-3. DOI: 10.1001/archneur.62.5.770
    [12]
    BUERGER K, TEIPEL S J, ZINKOWSKI R, et al. CSF tau protein phosphorylated at threonine 231 correlates with cognitive decline in MCI subjects[J]. Neurology, 2002, 59(4): 627-629. doi: 10.1212/WNL.59.4.627
    [13]
    JANELIDZE S, STOMRUD E, SMITH R, et al. Cerebrospinal fluid p-tau217 performs better than p-tau181 as a biomarker of Alzheimer's disease[J]. Nat Commun, 2020, 11(1): 1683. doi: 10.1038/s41467-020-15436-0
    [14]
    BARTHELEMY N R, BATEMAN R J, HIRTZ C, 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[J]. Alzheimers Res Ther, 2020, 12(1): 26. doi: 10.1186/s13195-020-00596-4
    [15]
    LANTERO-RODRIGUEZ J, SNELLMAN A, BENEDET A L, et al. P-tau235: a novel biomarker for staging preclinical Alzheimer's disease[J]. EMBO Mol Med, 2021, 13(12): e15098. DOI: 10.15252/emmm.202115098.
    [16]
    KANDALEPAS P C, SADLEIR K R, EIMER W A, et al. The Alzheimer's beta-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques[J]. Acta Neuropathol, 2013, 126(3): 329-352. doi: 10.1007/s00401-013-1152-3
    [17]
    ZETTERBERG H, ANDREASSON U, HANSSON O, et al. Elevated cerebrospinal fluid BACE1 activity in incipient Alzheimer disease[J]. Arch Neurol, 2008, 65(8): 1102-1107.
    [18]
    ZHONG Z, EWERS M, TEIPEL S, et al. Levels of beta-secretase (BACE1) in cerebrospinal fluid as a predictor of risk in mild cognitive impairment[J]. Arch Gen Psychiatry, 2007, 64(6): 718-726. doi: 10.1001/archpsyc.64.6.718
    [19]
    VERHEIJEN J H, HUISMAN L G, van LENT N, et al. Detection of a soluble form of BACE1 in human cerebrospinal fluid by a sensitive activity assay[J]. Clin Chem, 2006, 52(6): 1168-1174. doi: 10.1373/clinchem.2006.066720
    [20]
    ROSEN C, ANDREASSON U, MATTSSON N, et al. Cerebrospinal fluid profiles of amyloid beta-related biomarkers in Alzheimer's disease[J]. Neuromolecular Med, 2012, 14(1): 65-73. doi: 10.1007/s12017-012-8171-4
    [21]
    HOLSINGER R M, LEE J S, BOYD A, et al. CSF BACE1 activity is increased in CJD and Alzheimer's disease versus[corrected] other dementias[J]. Neurology, 2006, 67(4): 710-712. doi: 10.1212/01.wnl.0000229925.52203.4c
    [22]
    MULDER S D, van der FLIER W M, VERHEIJEN J H, et al. BACE1 activity in cerebrospinal fluid and its relation to markers of AD pathology[J]. J Alzheimers Dis, 2010, 20(1): 253-260. doi: 10.3233/JAD-2010-1367
    [23]
    CHOURAKI V, BEISER A, YOUNKIN L, et al. Plasma amyloid-beta and risk of Alzheimer's disease in the Framingham Heart Study[J]. Alzheimers Dement, 2015, 11(3): 249-257. doi: 10.1016/j.jalz.2014.07.001
    [24]
    van OIJEN M, HOFMAN A, SOARES H D, et al. Plasma Abeta(1-40) and Abeta(1-42) and the risk of dementia: a prospective case-cohort study[J]. Lancet Neurol, 2006, 5(8): 655-660. doi: 10.1016/S1474-4422(06)70501-4
    [25]
    ABDULLAH L, LUIS C, PARIS D, et al. Serum Abeta levels as predictors of conversion to mild cognitive impairment/Alzheimer disease in an ADAPT subcohort[J]. Mol Med, 2009, 15(11-12): 432-437. doi: 10.2119/molmed.2009.00083
    [26]
    HANSSON O, ZETTERBERG H, VANMECHELEN E, et al. Evaluation of plasma Aβ40 and Aβ42 as predictors of conversion to Alzheimer's disease in patients with mild cognitive impairment[J]. Neurobiol Aging, 2010, 31(3): 357-367. doi: 10.1016/j.neurobiolaging.2008.03.027
    [27]
    LOPEZ O L, KULLER L H, MEHTA P D, et al. Plasma amyloid levels and the risk of AD in normal subjects in the cardiovascular health study[J]. Neurology, 2008, 70(19): 1664-1671. doi: 10.1212/01.wnl.0000306696.82017.66
    [28]
    LOVHEIM H, ELGH F, JOHANSSON A, et al. Plasma concentrations of free amyloid beta cannot predict the development of Alzheimer's disease[J]. Alzheimers Dement, 2017, 13(7): 778-782. doi: 10.1016/j.jalz.2016.12.004
    [29]
    TOSUN D, VEITCH D, AISEN P, et al. Detection of β-amyloid positivity in Alzheimer's disease neuroimaging initiative participants with demographics, cognition, MRI and plasma biomarkers[J]. Brain Communications, 2021, 3(2). DOI: 10.1093/braincomms/fcab008.
    [30]
    QU Y, MA Y H, HUANG Y Y, et al. Blood biomarkers for the diagnosis of amnestic mild cognitive impairment and Alzheimer's disease: a systematic review and meta-analysis[J]. Neurosci Biobehav Rev, 2021, 128: 479-486. doi: 10.1016/j.neubiorev.2021.07.007
    [31]
    SIMREN J, LEUZY A, KARIKARI T K, et al. The diagnostic and prognostic capabilities of plasma biomarkers in Alzheimer's disease[J]. Alzheimers Dement, 2021, 17(7): 1145-1156. doi: 10.1002/alz.12283
    [32]
    MIELKE M M, HAGEN C E, WENNBERG A, et al. Association of plasma total tau level with cognitive decline and risk of mild cognitive impairment or dementia in the Mayo clinic study on aging[J]. JAMA Neurol, 2017, 74(9): 1073-1080. doi: 10.1001/jamaneurol.2017.1359
    [33]
    MIELKE M M, HAGEN C E, XU J, et al. Plasma phospho-tau181 increases with Alzheimer's disease clinical severity and is associated with tau-and amyloid-positron emission tomography[J]. Alzheimers Dement, 2018, 14(8): 989-997. doi: 10.1016/j.jalz.2018.02.013
    [34]
    MATTSSON-CARLGREN N, JANELIDZE S, PALMQVIST S, et al. Longitudinal plasma p-tau217 is increased in early stages of Alzheimer's disease[J]. Brain, 2020, 143(11): 3234-3241. doi: 10.1093/brain/awaa286
    [35]
    PALMQVIST S, JANELIDZE S, QUIROZ Y T, et al. Discriminative accuracy of plasma phospho-tau217 for Alzheimer disease vs other neurodegenerative disorders[J]. JAMA, 2020, 324(8): 772-781. doi: 10.1001/jama.2020.12134
    [36]
    JANELIDZE S, MATTSSON N, PALMQVIST S, et al. Plasma P-tau181 in Alzheimer's disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer's dementia[J]. Nat Med, 2020, 26(3): 379-386. doi: 10.1038/s41591-020-0755-1
    [37]
    MATTSSON N, ANDREASSON U, ZETTERBERG H, et al. Association of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease[J]. JAMA Neurol, 2017, 74(5): 557-566. doi: 10.1001/jamaneurol.2016.6117
    [38]
    MATTSSON N, CULLEN N C, ANDREASSON U, et al. Association between longitudinal plasma neurofilament light and neurodegeneration in patients with Alzheimer disease[J]. JAMA Neurol, 2019, 76(7): 791-799. doi: 10.1001/jamaneurol.2019.0765
    [39]
    PREISCHE O, SCHULTZ S A, APEL A, et al. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer's disease[J]. Nat Med, 2019, 25(2): 277-283. doi: 10.1038/s41591-018-0304-3
    [40]
    LU Y, TAN L, WANG X. Circular HDAC9/microRNA-138/Sirtuin-1 pathway mediates synaptic and amyloid precursor protein processing deficits in Alzheimer's disease[J]. Neurosci Bull, 2019, 35(5): 877-888. doi: 10.1007/s12264-019-00361-0
    [41]
    GEEKIYANAGE H, JICHA G A, NELSON P T, et al. Blood serum miRNA: non-invasive biomarkers for Alzheimer's disease[J]. Exp Neurol, 2012, 235(2): 491-496. doi: 10.1016/j.expneurol.2011.11.026
    [42]
    XIE B, LIU Z, JIANG L, et al. Increased serum miR-206 level predicts conversion from amnestic mild cognitive impairment to Alzheimer's disease: a 5-year follow-up study[J]. J Alzheimers Dis, 2017, 55(2): 509-520.
    [43]
    DURAND D, CARNIGLIA L, TURATI J, et al. Amyloid-beta neurotoxicity and clearance are both regulated by glial group Ⅱ metabotropic glutamate receptors[J]. Neuropharmacology, 2017, 123: 274-286. doi: 10.1016/j.neuropharm.2017.05.008
    [44]
    XIE B, ZHOU H, LIU W, et al. Evaluation of the diagnostic value of peripheral BDNF levels for Alzheimer's disease and mild cognitive impairment: results of a meta-analysis[J]. Int J Neurosci, 2020, 130(3): 218-230. doi: 10.1080/00207454.2019.1667794
    [45]
    BERTRAM L, TANZI R E. Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses[J]. Nat Rev Neurosci, 2008, 9(10): 768-778. doi: 10.1038/nrn2494
    [46]
    TANZI R E, BERTRAM L. Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective[J]. Cell, 2005, 120(4): 545-555. doi: 10.1016/j.cell.2005.02.008
    [47]
    MCKHANN G M, KNOPMAN D S, CHERTKOW H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease[J]. Alzheimers Dement, 2011, 7(3): 263-269. doi: 10.1016/j.jalz.2011.03.005
    [48]
    LI J Q, TAN L, WANG H F, et al. Risk factors for predicting progression from mild cognitive impairment to Alzheimer's disease: a systematic review and meta-analysis of cohort studies[J]. J Neurol Neurosurg Psychiatry, 2016, 87(5): 476-484. doi: 10.1136/jnnp-2014-310095
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