Using Memory Strength to Shift Response Bias in Patients With Amnestic Mild Cognitive Impairment and Alzheimer's Disease

2014 ◽  
Author(s):  
Michael Tat ◽  
Rebecca Deason ◽  
Sean Flannery ◽  
Emma Gosselin ◽  
Andrew Budson
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.


2014 ◽  
Vol 11 (2) ◽  
pp. 200-205
Author(s):  
Aleksandra Klimkowicz-Mrowiec ◽  
Lukasz Krzywoszanski ◽  
Karolina Spisak ◽  
Bryan Donohue ◽  
Andrzej Szczudlik ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e105623 ◽  
Author(s):  
Katerina Sheardova ◽  
Jan Laczó ◽  
Martin Vyhnalek ◽  
Ross Andel ◽  
Ivana Mokrisova ◽  
...  

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