scholarly journals Prediction and Classification of Alzheimer’s Disease Based on Combined Features From Apolipoprotein-E Genotype, Cerebrospinal Fluid, MR, and FDG-PET Imaging Biomarkers

Author(s):  
Yubraj Gupta ◽  
Ramesh Kumar Lama ◽  
Goo-Rak Kwon ◽  
2013 ◽  
Vol 124 (11) ◽  
pp. 2146-2152 ◽  
Author(s):  
F. Hatz ◽  
N. Benz ◽  
M. Hardmeier ◽  
R. Zimmermann ◽  
S. Rueegg ◽  
...  

2020 ◽  
Vol 40 (4) ◽  
pp. 545-554
Author(s):  
Bang-Hung Yang ◽  
Jyh-Cheng Chen ◽  
Wen-Hsiang Chou ◽  
Wen-Sheng Huang ◽  
Jong-Ling Fuh ◽  
...  

2018 ◽  
Vol 15 (13) ◽  
pp. 1267-1275 ◽  
Author(s):  
F.E. Reesink ◽  
D. Vállez García ◽  
C.A. Sánchez-Catasús ◽  
D.E. Peretti ◽  
A.T. Willemsen ◽  
...  

Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.


2006 ◽  
Vol 2 ◽  
pp. S179-S179
Author(s):  
Jonathan M. Schott ◽  
Basil H. Ridha ◽  
Sebastian J. Crutch ◽  
Elizabeth K. Warrington ◽  
Martin N. Rossor ◽  
...  

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