P4-214: Progression of Mild Cognitive Impairment Due to Alzheimer's Disease With Amyloid-PET and FDG-PET Imaging

2016 ◽  
Vol 12 ◽  
pp. P1109-P1109
Author(s):  
Shizuo Hatashita ◽  
Hidetomo Yamasaki ◽  
Daichi Wakebe
2021 ◽  
Author(s):  
Camilla Caprioglio ◽  
Valentina Garibotto ◽  
Frank Jessen ◽  
Lutz Frölich ◽  
Gilles Allali ◽  
...  

Abstract Background. This study aims to investigate the clinical use of the main Alzheimer’s disease (AD) biomarkers in patients with mild cognitive impairment (MCI) by examining the beliefs and preferences of clinicians and biomarker experts of the European Alzheimer’s Disease Consortium (EADC).Methods. Out of 306 contacted EADC professionals, 150 (101 clinicians, 43 biomarker experts, and 6 falling into other categories) filled in an online survey from May to September 2020. The investigated biomarkers were: medial temporal lobe atrophy score (MTA) on structural MRI, typical AD (i.e. temporoparietal and posterior cingulate) hypometabolism on FDG-PET, CSF (Aβ42, p-tau, t-tau), amyloid-PET and tau-PET.Results. Despite the abnormal accumulation of amyloid rather than tau was deemed by the majority of responders as the initial cause of AD, responders did not show a clear preference for amyloid-PET. The most widely used biomarker is MTA (77% of responders reported to use it at least frequently), followed by Aβ42, p-tau, t-tau levels in CSF (45%), typical AD hypometabolism on FDG-PET (32%), amyloid-PET (8%), and tau-PET (2%). Imaging and CSF biomarkers were found to be widely used to support the etiological diagnostic process in MCI, while APOE genotyping was performed only in a minority of patients. CSF is considered the most valuable biomarker in terms of additional diagnostic value, followed by amyloid-PET, tau-PET, and typical AD hypometabolism on FDG-PET. The combination of amyloidosis and neuronal injury biomarkers is associated with the highest diagnostic confidence in an etiological diagnosis of AD in MCI, while MTA alone was perceived as the less reliable biomarker.Conclusions. Biomarkers are widely used across Europe for the diagnosis of MCI. Overall, we observed that CSF is currently considered as the most useful biomarker, followed by amyloid-PET. Moreover, the use of molecular imaging (i.e. amyloid-PET and tau-PET) in the diagnostic work-up of MCI patients is increasing over time.


2009 ◽  
Vol 257 (5) ◽  
pp. 721-727 ◽  
Author(s):  
Katsutoshi Furukawa ◽  
Nobuyuki Okamura ◽  
Manabu Tashiro ◽  
Masaaki Waragai ◽  
Shozo Furumoto ◽  
...  

2015 ◽  
Vol 47 (3) ◽  
pp. 539-543 ◽  
Author(s):  
Solveig Tiepolt ◽  
Marianne Patt ◽  
Karl-Titus Hoffmann ◽  
Matthias L. Schroeter ◽  
Osama Sabri ◽  
...  

2015 ◽  
Vol 11 (7S_Part_8) ◽  
pp. P400-P400
Author(s):  
Woon Yeong Park ◽  
Sang Hoon Kim ◽  
Sang Hag Park ◽  
Seung Gon Kim ◽  
Shin Young Park ◽  
...  

2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.


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