Journal of Internal Medicine Concepts & Practice >

2023 , Vol. 18 >Issue 06: 447 - 450

DOI: https://doi.org/10.16138/j.1673-6087.2023.06.013

Review article

Current status and research progress of subjective cognitive decline in Alzheimer’s disease of preclinical stage

Expand

Received date: 2023-04-21

  Online published: 2024-03-18

Fold

Cite this article

YAO Minyi, LIU Yonglin . Current status and research progress of subjective cognitive decline in Alzheimer’s disease of preclinical stage[J]. Journal of Internal Medicine Concepts & Practice, 2023 , 18(06) : 447 -450 . DOI: 10.16138/j.1673-6087.2023.06.013

References

[1] Wang J, Wang K, Liu T, et al. Abnormal dynamic functional networks in subjective cognitive decline and Alzheimer’s disease[J]. Front Comput Neurosci, 2022, 16: 885126.
[2] Atri A. The Alzheimer’s disease clinical spectrum[J]. Med Clin North Am, 2019, 103(2): 263-293.
[3] Wang X, Huang W, Su L, et al. Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer’s disease[J]. Mol Neurodegener, 2020, 15(1):55.
[4] Jessen F, Amariglio RE, Buckley RF, et al. The characterisation of subjective cognitive decline[J]. Lancet Neurol, 2020, 19(3): 271-278.
[5] Jack CR Jr, Bennett DA, Blennow K, et al. NIA-AA research framework: toward a biological definition of Alzheimer’s disease[J]. Alzheimers Dement, 2018, 14(4):535-562.
[6] Mitchell A J, Beaumont H, Ferguson D, et al. Risk of dementia and mild cognitive impairment in older people with subjective memory complaints: meta-analysis[J]. Acta Psychiatr Scand, 2014, 130(6): 439-451.
[7] Slot RER, Sikkes SAM, Berkhof J, et al. Subjective cognitive decline and rates of incident Alzheimer’s disease and non-Alzheimer’s disease dementia[J]. Alzheimers Dement, 2019, 15(3): 465-476.
[8] Jia F, Li Y, Li M, et al. Subjective cognitive decline, cognitive reserve indicators, and the incidence of dementia[J]. J Am Med Dir Assoc, 2021, 22(7): 1449-1455.
[9] Oliver MD, Morrison C, Kamal F, et al. Subjective cognitive decline is a better marker for future cognitive decline in females than in males[J]. Alzheimers Res Ther, 2022, 14(1): 197.
[10] Ribaldi F, Rolandi E, Vaccaro R, et al. The clinical heterogeneity of subjective cognitive decline: a data-driven approach on a population-based sample[J]. Age Ageing, 2022, 51(10): afac209.
[11] Scheef L, Grothe MJ, Koppara A, et al. Subregional volume reduction of the cholinergic forebrain in subjective cognitive decline(SCD)[J]. Neuroimage Clin, 2019, 21:101612.
[12] Zhao W, Wang X, Yin C, et al. Trajectories of the hippocampal subfields atrophy in the Alzheimer’s disease[J]. Front Neuroinform, 2019, 13: 13.
[13] Chen Y, Wang Y, Song Z, et al. Abnormal white matter changes in Alzheimer’s disease based on diffusion tensor imaging[J]. Ageing Res Rev, 2023, 87: 101911.
[14] Wen Q, Mustafi SM, Li J, et al. White matter alterations in early-stage Alzheimer’s disease[J]. Alzheimers Dement (Amst), 2019, 11:576-587.
[15] Ryu SY, Lim EY, Na S, et al. Hippocampal and entorhinal structures in subjective memory impairment[J]. Int Psychogeriatr, 2017, 29(5): 785-792.
[16] Brueggen K, Dyrba M, Cardenas-Blanco A, et al. Structural integrity in subjective cognitive decline, mild cognitive impairment and Alzheimer’s disease based on multicenter diffusion tensor imaging[J]. J Neurol, 2019, 266(10): 2465-2474.
[17] Selnes P, Fjell AM, Gjerstad L, et al. White matter imaging changes in subjective and mild cognitive impairment[J]. Alzheimers Dement, 2012, 8(5 Suppl): S112-S121.
[18] Mohammadian F, Zare Sadeghi A, Noroozian M, et al. Quantitative assessment of resting-state functional connectivity MRI to differentiate amnestic mild cognitive impairment, late-onset Alzheimer’s disease from normal subjects[J]. J Magn Reson Imaging, 2023, 57(6): 1702-1712.
[19] Kucikova L, Goerdten J, Dounavi ME, et al. Resting-state brain connectivity in healthy young and middle-aged adults at risk of progressive Alzheimer’s disease[J]. Neurosci Biobehav Rev, 2021, 129: 142-153.
[20] Greicius MD, Krasnow B, Reiss AL, et al. Functional connectivity in the resting brain: a network analysis of the default mode hypothesis[J]. Proc Natl Acad Sci U S A, 2003, 100(1): 253-258.
[21] Jobson DD, Hase Y, Clarkson AN, et al. The role of the medial prefrontal cortex in cognition, ageing and dementia[J]. Brain Commun, 2021, 3(3): fcab125.
[22] Spreng RN, Turner GR. The shifting architecture of cognition and brain function in older adulthood[J]. Perspect Psychol Sci, 2019, 14(4): 523-542.
[23] Sun Y, Dai Z, Li Y, et al. Subjective cognitive decline: mapping functional and structural brain changes-A combined resting-state functional and structural MR imaging study[J]. Radiology, 2016, 281(1): 185-192.
[24] Yang L, Yan Y, Wang Y, et al. Gradual disturbances of the amplitude of low-frequency fluctuations(ALFF) and fractional ALFF in Alzheimer spectrum[J]. Front Neurosci, 2018, 12: 975.
[25] Viviano RP, Hayes JM, Pruitt PJ, et al. Aberrant memory system connectivity and working memory performance in subjective cognitive decline[J]. Neuroimage, 2019, 185: 556-564.
[26] Dillen KNH, Jacobs HIL, Kukolja J, et al. Aberrant functional connectivity differentiates retrosplenial cortex from posterior cingulate cortex in prodromal Alzheimer’s disease[J]. Neurobiol Aging, 2016, 44:114-126.
[27] Mak E, Bethlehem RAI, Romero-Garcia R, et al. In vivo coupling of tau pathology and cortical thinning in Alzheimer’s disease[J]. Alzheimers Dement (Amst), 2018, 10: 678-687.
[28] Ersoezlue E, Rauchmann BS, Schneider-Axmann T, et al. Lifelong experiences as a proxy of cognitive reserve moderate the association between connectivity and cognition in Alzheimer’s disease[J]. Neurobiol Aging, 2023, 122: 33-44.
[29] Parker AF, Smart CM, Scarapicchia V, et al. Identification of earlier biomarkers for Alzheimer’s disease: a multimodal neuroimaging study of individuals with subjective cognitive decline[J]. J Alzheimers Dis, 2020, 77(3): 1067-1076.
[30] Chen H, Sheng X, Luo C, et al. The compensatory phenomenon of the functional connectome related to pathological biomarkers in individuals with subjective cognitive decline[J]. Transl Neurodegener, 2020, 9(1): 21.
[31] Bao YW, Shea YF, Chiu PK, et al. The fractional amplitude of low-frequency fluctuations signals related to amyloid uptake in high-risk populations[J]. Front Aging Neurosci, 2022, 14: 956222.
[32] Sharma N, Murari G, Vandermorris S, et al. Functional connectivity between the posterior default mode network and parahippocampal gyrus is disrupted in older adults with subjective cognitive decline and correlates with subjective memory ability[J]. J Alzheimers Dis, 2021, 82(1): 435-445.
[33] Schwarz C, Benson GS, Antonenko D, et al. Negative affective burden is associated with higher resting-state functional connectivity in subjective cognitive decline[J]. Sci Rep, 2022, 12(1): 6212.
[34] Dhiman K, Blennow K, Zetterberg H, et al. Cerebrospinal fluid biomarkers for understanding multiple aspects of Alzheimer’s disease pathogenesis[J]. Cell Mol Life Sci, 2019, 76(10):1833-1863.
[35] Wen C, Bi YL, Hu H, et al. Association of subjective cognitive decline with cerebrospinal fluid biomarkers of Alzheimer’s disease pathology in cognitively intact older adults[J]. J Alzheimers Dis, 2022, 85(3): 1143-1151.
[36] Cicognola C, Hansson O, Scheltens P, et al. Cerebrospinal fluid N-224 tau helps discriminate Alzheimer’s disease from subjective cognitive decline and other dementias[J]. Alzheimers Res Ther, 2021, 13(1): 38.
[37] Mantzavinos V, Alexiou A. Biomarkers for Alzheimer’s disease diagnosis[J]. Curr Alzheimer Res, 2017, 14(11):1149-1154.
[38] Zetterberg H, Blennow K. Moving fluid biomarkers for Alzheimer’s disease from research tools to routine clinical diagnostics[J]. Mol Neurodegener, 2021, 16(1): 10.
[39] Prins S, Zhuparris A, Groeneveld GJ. Usefulness of plasma amyloid as a prescreener for the earliest Alzheimer pathological changes depends on the study population[J]. Ann Neurol, 2020, 87(1): 154-155.
[40] Wang X, Zhao M, Lin L, et al. Plasma β-amyloid levels associated with structural integrity based on diffusion tensor imaging in subjective cognitive decline[J]. Front Aging Neurosci, 2021, 12: 592024.
[41] Müller S, Preische O, G?pfert JC, et al. Tau plasma levels in subjective cognitive decline: results from the DELCODE study[J]. Sci Rep, 2017, 7(1): 9529.
[42] Verberk IMW, Thijssen E, Koelewijn J, et al. Combination of plasma amyloid beta(1-42/1-40) and glial fibrillary acidic protein strongly associates with cerebral amyloid pathology[J]. Alzheimers Res Ther, 2020, 12(1): 118.
[43] Rusek M, Pluta R, U?amek-Kozio? M, et al. Ketogenic diet in Alzheimer’s disease[J]. Int J Mol Sci, 2019, 20(16):3892.
[44] Tao Y, Leng SX, Zhang H. Ketogenic diet: an effective treatment approach for neurodegenerative diseases[J]. Curr Neuropharmacol, 2022, 20(12): 2303-2319.
[45] Danial NN, Hartman AL, Stafstrom CE, et al. How does the ketogenic diet work?[J]. J Child Neurol, 2013, 28(8): 1027-1033.
[46] Neth BJ, Mintz A, Whitlow C, et al. Modified ketogenic diet is associated with improved cerebrospinal fluid biomarker profile, cerebral perfusion, and cerebral ketone body uptake in older adults at risk for Alzheimer’s disease[J]. Neurobiol Aging, 2020, 86: 54-63.
[47] Chong TWH, Curran E, Ellis KA, et al. Physical activity for older Australians with mild cognitive impairment or subjective cognitive decline[J]. J Sci Med Sport, 2020, 23(10): 913-920.
Options
Outlines

/

〈 〉