scholarly journals Use of MRI cortical thickness, FDG PET, and PIB (Pittsburgh B) PET imaging to distinguish atypical Alzheimer's Disease and frontotemporal dementia cases

2010 ◽  
Vol 4 ◽  
Author(s):  
Evans A.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Cortical Thickness ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Atypical Alzheimer’S Disease

P4-297: MR-LESS SURFACE-BASED [18 F]-FDG PET IMAGING DIFFERENTIATES FRONTOTEMPORAL DEMENTIA FROM ALZHEIMER'S DISEASE

2006 ◽  
Vol 14 (7S_Part_30) ◽  
pp. P1564-P1565
Author(s):  
Charles B. Malpas ◽  
Sarah Lee ◽  
Kirrily Rogers ◽  
David G. Darby ◽  
Michele Veldsman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Pet Imaging ◽  
Fdg Pet

Crossed Cerebellar Diaschisis in Alzheimer’s Disease

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 ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Left Hemisphere ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Pathophysiological Mechanism ◽  
Crossed Cerebellar Diaschisis ◽  
Amyloid Accumulation ◽  
Cerebellar Diaschisis ◽  
18F Fdg

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.

Cortical Thickness in Frontotemporal Dementia, Mild Cognitive Impairment, and Alzheimer's Disease

2012 ◽  
Vol 30 (4) ◽  
pp. 857-874 ◽  
Author(s):  
Päivi Hartikainen ◽  
Janne Räsänen ◽  
Valtteri Julkunen ◽  
Eini Niskanen ◽  
Merja Hallikainen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Frontotemporal Dementia ◽  
Cortical Thickness

scholarly journals FDG-PET improves accuracy in distinguishing frontotemporal dementia and Alzheimer's disease

Brain ◽  
2007 ◽  
Vol 130 (10) ◽  
pp. 2616-2635 ◽  
Author(s):  
N. L. Foster ◽  
J. L. Heidebrink ◽  
C. M. Clark ◽  
W. J. Jagust ◽  
S. E. Arnold ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Fdg Pet

scholarly journals Distribution of pathological hallmarks and association with post‐mortem MRI cortical thickness in typical and atypical Alzheimer’s disease

2020 ◽  
Vol 16 (S1) ◽  
Author(s):  
Laura E. Jonkman ◽  
Baayla D.C. Boon ◽  
Irene Frigerio ◽  
Martijn D. Steenwijk ◽  
Paolo Preziosa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Thickness ◽  
Post Mortem ◽  
Atypical Alzheimer’S Disease

scholarly journals P1-304: Changes in MRI cortical thickness and [18F]FDG PET data over 24 months in subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) Study

2011 ◽  
Vol 7 ◽  
pp. S207-S207 ◽  
Author(s):  
Arnaud Charil ◽  
Felix Carbonell ◽  
Anthonin Reilhac ◽  
Kristina Deduck ◽  
Rohit Sood ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Thickness ◽  
Fdg Pet ◽  
18F Fdg

scholarly journals Imaging beta-amyloid (Aβ) burden in the brains of middle-aged individuals with alcohol-use disorders: a [11C]PIB PET study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Margaret R. Flanigan ◽  
Sarah K. Royse ◽  
David P. Cenkner ◽  
Katelyn M. Kozinski ◽  
Clara J. Stoughton ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Alcohol Use ◽  
Cortical Thickness ◽  
Pet Imaging ◽  
Healthy Controls ◽  
Middle Aged ◽  
Neurocognitive Dysfunction ◽  
Amyloid Aβ

AbstractNo in vivo human studies have examined the prevalence of Alzheimer’s disease (AD) neuropathology in individuals with alcohol-use disorder (AUD), although recent research suggests that a relationship between the two exists. Therefore, this study used Pittsburgh Compound-B ([11C]PiB) PET imaging to test the hypothesis that AUD is associated with greater brain amyloid (Aβ) burden in middle-aged adults compared to healthy controls. Twenty healthy participants (14M and 6F) and 19 individuals with AUD (15M and 4F), all aged 40–65 years, underwent clinical assessment, MRI, neurocognitive testing, and positron emission tomography (PET) imaging. Global [11C]PiB standard uptake value ratios (SUVRs), cortical thickness, gray matter volumes (GMVs), and neurocognitive function in subjects with AUD were compared to healthy controls. These measures were selected because they are considered markers of risk for future AD and other types of neurocognitive dysfunction. The results of this study showed no significant differences in % global Aβ positivity or subthreshold Aβ loads between AUD and controls. However, relative to controls, we observed a significant 6.1% lower cortical thickness in both AD-signature regions and in regions not typically associated with AD, lower GMV in the hippocampus, and lower performance on tests of attention as well as immediate and delayed memory in individuals with AUD. This suggest that Aβ accumulation is not greater in middle-aged individuals with AUD. However, other markers of neurodegeneration, such as impaired memory, cortical thinning, and reduced hippocampal GMV, are present. Further studies are needed to elucidate the patterns and temporal staging of AUD-related pathophysiology and cognitive impairment. Imaging β-amyloid in middle age alcoholics as a mechanism that increases their risk for Alzheimer’s disease; Registration Number: NCT03746366.

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