参考文献/References:
[1] Jack CR, Bennett DA, Blennow K, et al. NIA-AA research framework: Toward a biological definition of Alzheimer’s disease[J]. Alzheimer’s & Dementia, 2018, 14(4):535-562.
[2] Jessen F, Amariglio RE, Van Boxtel M, et al. A conceptual framework for research on subjective cognitive decline in preclinical Alzheimer’s disease[J]. Alzheimers Dement, 2014, 10(6): 844-852.
[3] Jessen F, Amariglio RE, Buckley RF, et al. The characterisation of subjective cognitive decline[J]. Lancet Neurol, 2020, 19(3): 271-278.
[4] Mitchell AJ, 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.
[5] Slot R, Sikkes S, 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.
[6] Rabin LA, Smart CM, Amariglio RE. Subjective cognitive decline in preclinical alzheimer’s disease[J]. Annu Rev Clin Psychol, 2017, 13(1): 369-396.
[7] Wolfsgruber S, Kleineidam L, Guski J, et al. Minor neuropsychological deficits in patients with subjective cognitive decline[J]. Neurology, 2020, 95(9): e1134-e1143.
[8] Chen G, Yang K, Du W, et al. Clinical characteristics in subjective cognitive decline with and without worry: baseline investigation of the SILCODE study[J]. J Alzheimers Dis, 2019, 72(2): 443-454.
[9] Ryu SY, Kim A, Kim S, et al. Self- and informant-reported cognitive functioning and awareness in subjective cognitive decline, mild cognitive impairment, and very mild Alzheimer disease[J]. Int J Geriatr Psychiatry, 2020, 35(1): 91-98.
[10] Caselli RJ, Chen K, Locke DE, et al. Subjective cognitive decline: self and informant comparisons[J]. Alzheimers Dement, 2014, 10(1): 93-98.
[11] Liew TM. Trajectories of subjective cognitive decline, and the risk of mild cognitive impairment and dementia[J]. Alzheimers Res Ther, 2020, 12(1): 135.
[12] Snitz BE, Wang T, Cloonan YK, et al. Risk of progression from subjective cognitive decline to mild cognitive impairment: The role of study setting[J]. Alzheimers Dement, 2018, 14(6): 734-742.
[13] Blennow K, Hampel H, Weiner M, et al. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease[J]. Nat Rev Neurol, 2010, 6(3): 131-144.
[14] Sierra-Rio A, Balasa M, Olives J, et al. Cerebrospinal fluid biomarkers predict clinical evolution in patients with subjective cognitive decline and mild cognitive impairment[J]. Neurodegener Dis, 2016, 16(1/2): 69-76.
[15] Mandecka M, Budziszewska M, Barczak A, et al. Association between Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease, APOE Genotypes and Auditory Verbal Learning Task in Subjective Cognitive Decline, Mild Cognitive Impairment, and Alzheimer’s Disease[J]. J Alzheimers Dis, 2016, 54(1): 157-168.
[16] Wolfsgruber S, Polcher A, Koppara A, et al. Cerebrospinal fluid biomarkers and clinical progression in patients with subjective cognitive decline and mild cognitive impairment[J]. J Alzheimers Dis, 2017, 58(3): 939-950.
[17] Banning L, Ramakers I, K?ler S, et al. The association between biomarkers and neuropsychiatric symptoms across the alzheimer’s disease spectrum[J]. Am J Geriatr Psychiatry, 2020, 28(7): 735-744.
[18] Prins S, Zhuparris A, Gj G. 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.
[19] Verberk I, Hendriksen H, Van Harten AC, et al. Plasma amyloid is associated with the rate of cognitive decline in cognitively normal elderly: the SCIENCe project[J]. Neurobiol Aging, 2020, 89: 99-107.
[20] 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: the SILCODE study[J]. Front Aging Neurosci, 2020, 12: 592024.
[21] Stockmann J, Verberk I, Timmesfeld N, et al. Amyloid-β misfolding as a plasma biomarker indicates risk for future clinical Alzheimer’s disease in individuals with subjective cognitive decline[J]. Alzheimers Res Ther, 2020, 12(1): 169.
[22] Müller S, Preische O, G?fert JC, et al. Tau plasma levels in subjective cognitive decline: Results from the DELCODE study[J]. Sci Rep, 2017, 7(1): 9529.
[23] 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.
[24] Janelidze S, Berron D, Smith R, et al. Associations of plasma Phospho-Tau217 levels with Tau positron emission tomography in early alzheimer disease[J]. JAMA Neurol, 2021, 78(2): 149-156.
[25] Verberk I, 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.
[26] De Leeuw FA, Van Der Flier WM, Tijms BM, et al. Specific nutritional biomarker profiles in mild cognitive impairment and subjective cognitive decline are associated with clinical progression: the NUDAD project[J]. J Am Med Dir Assoc, 2020, 21(10): 1513.e1-1513.e17.
[27] Slot RER, Van Harten AC, Kester MI, et al. Apolipoprotein A1 in cerebrospinal fluid and plasma and progression to Alzheimer’s disease in non-demented elderly[J]. Journal of Alzheimer’s Disease, 2017, 56(2):687-697.
[28] Amaefule CO, Dyrba M, Wolfsgruber S, et al. Association between composite scores of domain-specific cognitive functions and regional patterns of atrophy and functional connectivity in the Alzheimer’s disease spectrum[J]. Neuroimage Clin, 2021, 29: 102533.
[29] Marcotte C, Potvin O, Collins DL, et al. Brain atrophy and patch-based grading in individuals from the CIMA-Q study: a progressive continuum from subjective cognitive decline to AD[J]. Sci Rep, 2019, 9(1): 13532.
[30] Yue L, Wang T, Wang J, et al. Asymmetry of hippocampus and amygdala defect in subjective cognitive decline among the community dwelling Chinese[J]. Front Psychiatry, 2018, 9: 226.
[31] Sun Y, Wang X, Wang Y, et al. Anxiety correlates with cortical surface area in subjective cognitive decline: APOE ε4 carriers versus APOE ε4 non-carriers[J]. Alzheimers Res Ther, 2019, 11(1): 50.
[32] Yang L, Yan Y, Li Y, et al. Frequency-dependent changes in fractional amplitude of low-frequency oscillations in Alzheimer’s disease: a resting-state fMRI study[J]. Brain Imaging Behav, 2020, 14(6): 2187-2201.
[33] Liang L, Zhao L, Wei Y, et al. Structural and functional hippocampal changes in subjective cognitive decline from the community[J]. Front Aging Neurosci, 2020, 12: 64.
[34] Li S, Daamen M, Scheef L, et al. Abnormal regional and global connectivity measures in subjective cognitive decline depending on cerebral amyloid status[J]. J Alzheimers Dis, 2021, 79(2): 493-509.
[35] Zhen D, Xia W, Zq Y, et al. Alterations of brain local functional connectivity in amnestic mild cognitive impairment[J]. Transl Neurodegener, 2018, 7(1): 26.
[36] Xu X, Li W, Tao M, et al. Effective and accurate diagnosis of subjective cognitive decline based on functional connection and graph theory view[J]. Front Neurosci, 2020, 14: 577887.
[37] Xu X, Li W, Mei J, et al. Feature selection and combination of information in the functional brain connectome for discrimination of mild cognitive impairment and analyses of altered brain patterns[J]. Front Aging Neurosci, 2020, 12: 28.
[38] 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.
[39] Luo C, Li M, Qin R, et al. White matter microstructural damage as an early sign of subjective cognitive decline[J]. Front Aging Neurosci, 2019, 11: 378.
[40] Shu N, Wang X, Bi Q, et al. Disrupted topologic efficiency of white matter structural connectome in individuals with subjective cognitive decline[J]. Radiology, 2018, 286(1): 229-238.
[41] Yan T, Wang W, Yang L, et al. Rich club disturbances of the human connectome from subjective cognitive decline to Alzheimer’s disease[J]. Theranostics, 2018, 8(12): 3237-3255.
[42] Scheef L, Spottke A, Daerr M, et al. Glucose metabolism, gray matter structure, and memory decline in subjective memory impairment[J]. Neurology, 2012, 79(13): 1332-1339.
[43] Song IU, Choi EK, Oh JK, et al. Alteration patterns of brain glucose metabolism: comparisons of healthy controls, subjective memory impairment and mild cognitive impairment[J]. Acta Radiol, 2016, 57(1): 90-97.
[44] Mosconi L, De Santi S, Brys M, et al. Hypometabolism and altered cerebrospinal fluid markers in normal apolipoprotein E E4 carriers with subjective memory complaints[J]. Biol Psychiatry, 2008, 63(6): 609-618.
[45] Dong QY, Li TR, Jiang XY, et al. Glucose metabolism in the right middle temporal gyrus could be a potential biomarker for subjective cognitive decline: a study of a Han population[J]. Alzheimers Res Ther, 2021, 13(1): 74.
[46] Buckley RF, Hanseeuw B, Schultz AP, et al. Region-Specific association of subjective cognitive decline with tauopathy Independent of global β-Amyloid burden[J]. JAMA Neurol, 2017, 74(12): 1455-1463.
[47] Timmers T, Ossenkoppele R, Verfaillie S, et al. Amyloid PET and cognitive decline in cognitively normal individuals: the SCIENCe project[J]. Neurobiol Aging, 2019, 79: 50-58.
[48] Bullich S, Roé-Vellvé N, Marquié M, et al. Early detection of amyloid load using 18F-florbetaben PET[J]. Alzheimers Res Ther, 2021, 13(1): 67.
[49] Ebenau JL, Verfaillie S, Van Den Bosch KA, et al. Grey zone amyloid burden affects memory function: the SCIENCe project[J]. Eur J Nucl Med Mol Imaging, 2021, 48(3): 747-756.