P4-308: [18F]FLUTEMETAMOL AMYLOID PET IMAGING: OUTCOME OF A PHASE III STUDY IN SUBJECTS WITH AMNESTIC MILD COGNITIVE IMPAIRMENT AFTER A 3-YEAR FOLLOW-UP

2014 ◽  
Vol 10 ◽  
pp. P898-P898 ◽  
Author(s):  
David A. Wolk ◽  
Ranjan Duara ◽  
Carl Sadowsky
Neurology ◽  
2011 ◽  
Vol 76 (12) ◽  
pp. 1085-1090 ◽  
Author(s):  
J. Koivunen ◽  
N. Scheinin ◽  
J. R. Virta ◽  
S. Aalto ◽  
T. Vahlberg ◽  
...  

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.


Neurocase ◽  
2017 ◽  
Vol 23 (1) ◽  
pp. 41-51 ◽  
Author(s):  
David A. Weidman ◽  
Edward Zamrini ◽  
Marwan N. Sabbagh ◽  
Sandra Jacobson ◽  
Anna Burke ◽  
...  

2013 ◽  
Vol 9 (4) ◽  
pp. e106-e109 ◽  
Author(s):  
Keith A. Johnson ◽  
Satoshi Minoshima ◽  
Nicolaas I. Bohnen ◽  
Kevin J. Donohoe ◽  
Norman L. Foster ◽  
...  

2013 ◽  
Vol 54 (7) ◽  
pp. 1011-1013 ◽  
Author(s):  
K. A. Johnson ◽  
S. Minoshima ◽  
N. I. Bohnen ◽  
K. J. Donohoe ◽  
N. L. Foster ◽  
...  

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