Progress of research on preclinical Alzheimer&rsquo;s disease based on functional MRI

SHENG Can1; LIU Fang1; HAN Ying2

Journal of China Clinic Medical Imaging ›› 2018, Vol. 29 ›› Issue (5) : 359-362.

Progress of research on preclinical Alzheimer’s disease based on functional MRI

SHENG Can1, LIU Fang1, HAN Ying2

Author information +

History +

Abstract

Alzheimer’s disease(AD) is considered as a continuously pathophysiological process. Special pathological changes of AD has occurred decades prior to the onset of clinical symptoms. Currently, due to the advanced neuroimaging techniques and biochemical tests, variant AD-related biomarkers are gradually identified, making it possible to diagnose AD in the preclinical stage and further intervene the process of the disease. Functional MRI(fMRI), which is helpful to reveal the early brain functional activities in preclinical AD, is the most common form of functional imaging techniques. This review is about researches involving preclinical AD based on fMRI in recent years.

Key words

Alzheimer disease / Magnetic resonance imaging

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

SHENG Can1, LIU Fang1, HAN Ying2. Progress of research on preclinical Alzheimer’s disease based on functional MRI[J]. Journal of China Clinic Medical Imaging. 2018, 29(5): 359-362

References

[1]Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of 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): 280-292.
[2]Dubois B, Hampel H, Feldman HH, et al. Preclinical Alzheimer's disease: Definition, natural history, and diagnostic criteria[J]. Alzheimers Dement, 2016, 12(3): 292-323.
[3]Wang J, Tan L, Yu JT. Prevention Trials in Alzheimer's Disease: Current Status and Future Perspectives[J]. J Alzheimers Dis, 2016, 50(4): 927-945.
[4]Biswal B, Yetkin FZ, Haughton VM, et al. Functional connectivity in the motor cortex of resting human brain using echo-planar MRI[J]. Magn Reson Med, 1995, 34(4): 537-541.
[5]李瑜霞，李永秋，孙宇，等. 源于阿尔茨海默病的轻度认知障碍患者脑结构及静息态功能磁共振研究进展[J]. 中国临床医学影像杂志，2016，27（2）：131-134.
[6]Selkoe DJ. Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior[J]. Behav Brain Res, 2008, 192(1): 106-113.
[7]Hedden T, Van Dijk KR, Becker JA, et al. Disruption of functional connectivity in clinically normal older adults harboring amyloid burden[J]. J Neurosci, 2009, 29(40): 12686-12694.
[8]Sheline YI, Price JL, Yan Z, et al. Resting-state functional MRI in depression unmasks increased connectivity between networks via the dorsal nexus[J]. Proc Natl Acad Sci USA, 2010, 107(24): 11020-11025.
[9]Dubois B, Feldman HH, Jacova C, et al. Research criteria for the diagnosis of Alzheimer’s disease: revising the NINCDS-ADRDA criteria[J]. Lancet Neurol, 2007, 6(8): 734-746.
[10]Dubois B, Feldman HH, Jacova C, et al. Revising the definition of Alzheimer's disease: a new lexicon[J]. Lancet Neurol, 2010, 9(11): 1118-1127.
[11]Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria[J]. Lancet Neurol, 2014, 13(6): 614-629.
[12]Jack CR, Knopman DS, Jagust WJ, et al. Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade[J]. Lancet Neurol, 2010, 9(1): 119-128.
[13]Jack CR, Vemuri P, Wiste HJ, et al. Evidence for ordering of Alzheimer disease biomarkers[J]. Arch Neurol, 2011, 68(12): 1526-1535.
[14]Besson FL, La Joie R, Doeuvre L, et al. Cognitive and Brain Profiles Associated with Current Neuroimaging Biomarkers of Preclinical Alzheimer's Disease[J]. J Neurosci, 2015, 35(29): 10402-10411.
[15]Sheline YI, Raichle ME. Resting state functional connectivity in preclinical Alzheimer's disease[J]. Biol Psychiatry, 2013, 74(5): 340-347.
[16]Jack CR, Holtzman DM. Biomarker modeling of Alzheimer's disease[J]. Neuron, 2013, 80(6): 1347-1358.
[17]Sperling RA, Dickerson BC, Pihlajamaki M, et al. Functional alterations in memory networks in early Alzheimer's disease[J]. Neuromolecular Med, 2010, 12(1): 27-43.
[18]Das SR, Pluta J, Mancuso L, et al. Increased functional connectivity within medial temporal lobe in mild cognitive impairment[J]. Hippocampus, 2013, 23(1): 1-6.
[19]Edelman K, Tudorascu D, Agudelo C, et al. Amyloid-Beta Deposition is Associated with Increased Medial Temporal Lobe Activation during Memory Encoding in the Cognitively Normal Elderly[J]. Am J Geriatr Psychiatry, 2017, 25(5): 551-560.
[20]Leal SL, Landau SM, Bell RK, et al. Hippocampal activation is associated with longitudinal amyloid accumulation and cognitive decline[J]. Elife, 2017, 6.
[21]Huijbers W, Mormino EC, Wigman SE, et al. Amyloid deposition is linked to aberrant entorhinal activity among cognitively normal older adults[J]. J Neurosci, 2014, 34(15): 5200-5210.
[22]Oh H, Jagust WJ. Frontotemporal network connectivity during memory encoding is increased with aging and disrupted by beta-amyloid[J]. J Neurosci, 2013, 33(47): 18425-18437.
[23]Oh H, Steffener J, Razlighi QR, et al. Aβ-related hyperactivation in frontoparietal control regions in cognitively normal elderly[J]. Neurobiol Aging, 2015, 36(12): 3247-3254.
[24]Oh H, Steffener J, Razlighi QR, et al. β-Amyloid Deposition Is Associated with Decreased Right Prefrontal Activation during Task Switching among Cognitively Normal Elderly[J]. J Neurosci, 2016, 36(6): 1962-1970.
[25]Supekar K, Menon V, Rubin D, et al. Network analysis of intrinsic functional brain connectivity in Alzheimer's disease[J]. PLoS Comput Biol, 2008, 4(6): e1000100.
[26]Sheline YI, Raichle ME, Snyder AZ, et al. Amyloid plaques disrupt resting state default mode network connectivity in cognitively normal elderly[J]. Biol Psychiatry, 2010, 67(6): 584-587.
[27]Song Z, Insel PS, Buckley S, et al. Brain amyloid-β burden is associated with disruption of intrinsic functional connectivity within the medial temporal lobe in cognitively normal elderly[J]. J Neurosci, 2015, 35(7): 3240-3247.
[28]Buckner RL, Sepulcre J, Talukdar T, et al. Cortical hubs revealed by intrinsic functional connectivity: mapping, assessment of stability, and relation to Alzheimer's disease[J]. J Neurosci, 2009, 29(6): 1860-1873.
[29]Krajcovicova L, Marecek R, Mikl M, et al. Disruption of resting functional connectivity in Alzheimer's patients and at-risk subjects[J]. Curr Neurol Neurosci Rep, 2014, 14(10): 491.
[30]Simic G, Babic M, Borovecki F, et al. Early failure of the default-mode network and the pathogenesis of Alzheimer's disease[J]. CNS Neurosci Ther, 2014, 20(7): 692-698.
[31]Elman JA, Madison CM, Baker SL, et al. Effects of Beta-Amyloid on Resting State Functional Connectivity Within and Between Networks Reflect Known Patterns of Regional Vulnerability[J]. Cereb Cortex, 2016, 26(2): 695-707.
[32]Drzezga A, Becker JA, Van Dijk KR, et al. Neuronal dysfunction and disconnection of cortical hubs in non-demented subjects with elevated amyloid burden[J]. Brain, 2011, 134(Pt 6): 1635-1646.
[33]Schultz AP, Chhatwal JP, Hedden T, et al. Phases of Hyperconnectivity and Hypoconnectivity in the Default Mode and Salience Networks Track with Amyloid and Tau in Clinically Normal Individuals[J]. J Neurosci, 2017, 37(16): 4323-4331.
[34]Gordon BA, Zacks JM, Blazey T, et al. Task-evoked fMRI changes in attention networks are associated with preclinical Alzheimer's disease biomarkers[J]. Neurobiol Aging, 2015, 36(5): 1771-1779.
[35]盛灿，夏明睿，韩璎. 遗忘型轻度认知障碍的静息态功能MRI研究进展[J]. 中国临床医学影像杂志，2015，26（7）：528-530.
[36]Sheline YI, Morris JC, Snyder AZ, et al. APOE4 allele disrupts resting state fMRI connectivity in the absence of amyloid plaques or decreased CSF Abeta42[J]. J Neurosci， 2010， 30(50): 17035-17040.