Differential patterns of regional cerebral hypometabolism according to the level of cerebral amyloid deposition in patients with amnestic mild cognitive impairment

2016 ◽  
Vol 632 ◽  
pp. 104-108 ◽  
Author(s):  
So Yeon Jeon ◽  
Dahyun Yi ◽  
Min Soo Byun ◽  
Hyo Jung Choi ◽  
Hyun Jung Kim ◽  
...  
2018 ◽  
Author(s):  
Ileana O Jelescu ◽  
Timothy M Shepherd ◽  
Dmitry S Novikov ◽  
Yu-Shin Ding ◽  
Benjamin Ades-Aron ◽  
...  

The spatial-temporal relationships between gray and white matter (WM) degeneration during preclinical and early symptomatic Alzheimer's disease are poorly understood. We characterized β-amyloid deposition, cortical volume and WM degeneration in 44 subjects including healthy control (N=23), amnestic mild cognitive impairment (aMCI) (N=19), and early Alzheimer's subjects (N=2). Integrated PET-MRI provided simultaneous measurement of 18F-Florbetapir uptake in cortical areas, regional brain volumes from structural MRI, and WM tract integrity metrics from diffusion MRI using biophysical modeling. Across the cohort of healthy control and aMCIs, cortical volumes correlated poorly with β-amyloid deposition in the same area (p < 0.05 only in the posterior cingulate and parietal lobe). WM degeneration correlated significantly with both amyloid and volume of connected cortical areas, but more strongly with volume. Diffusion MRI metrics for WM demyelination and/or axonal loss could therefore provide new biomarkers associated with clinical Alzheimer's conversion. These WM changes may represent sequential propagation of Alzheimer's neurodegeneration between functionally connected regions, and/or evidence of direct WM injury during the Alzheimer's pathology cascade.


2021 ◽  
Vol 18 ◽  
Author(s):  
Yue Wang ◽  
Fanghua Lou ◽  
Yonggang Li ◽  
Fang Liu ◽  
Ying Wang ◽  
...  

Background: A significant proportion of patients with clinically diagnosed Alzheimer’s disease (AD) and an even higher proportion of patients with amnestic mild cognitive impairment (aMCI) do not show evidence of amyloid deposition on positron emission tomography (PET) with amyloid-binding tracers such as 11C-labeled Pittsburgh Compound B (PiB). Objective: This study aimed to identify clinical, neuropsychological and neuroimaging factors that might suggest amyloid neuropathology in patients with clinically suspected AD or aMCI. Methods: Forty patients with mild to moderate AD and 23 patients with aMCI who were clinically diagnosed in our memory clinic and had PiB PET scans were included. Clinical, neuropsychologi- cal, and imaging characteristics, such as medial temporal lobe atrophy (MTA) and white matter hy- perintensities (WMH) on MRI and metabolic pattern on 18F-labeled fluorodeoxyglucose (FDG) PET, were compared between patients with PiB positive and negative PET results for AD, aMCI, and all subjects combined, respectively. Results: Compared with PiB positive patients, PiB negative patients had a higher prevalence of hy- pertension history, better performance on the Mini-Mental State Examination, the Rey Auditory Verbal Learning Test, and the Judgement of Line Orientation, lower score of MTA, and were less likely to have temporoparietal-predominant hypometabolism on FDG PET. Affective symptoms were less common in PiB negative patients diagnosed with AD, and the Animal Fluency Test score was higher in PiB negative patients diagnosed with aMCI. Conclusion: : In patients with clinically diagnosed AD or aMCI, absence of a history of hyperten- sion, deficits in verbal learning and memory, visuospatial function, semantic verbal fluency, pres- ence of affective symptoms, MTA on MRI, and temporoparietal hypometabolism on FDG PET suggested amyloid deposition in the brain.


2016 ◽  
Vol 12 ◽  
pp. P724-P725
Author(s):  
So Yeon Jeon ◽  
Dahyun Yi ◽  
Min Soo Byun ◽  
Hyo Jung Choi ◽  
Hyun Jung Kim ◽  
...  

2021 ◽  
Vol 13 ◽  
Author(s):  
Lars Michels ◽  
Florian Riese ◽  
Rafael Meyer ◽  
Andrea M. Kälin ◽  
Sandra E. Leh ◽  
...  

Cognitive impairment indicates disturbed brain physiology which can be due to various mechanisms including Alzheimer's pathology. Combined functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) recordings (EEG-fMRI) can assess the interplay between complementary measures of brain activity and EEG changes to be localized to specific brain regions. We used a two-step approach, where we first examined changes related to a syndrome of mild cognitive impairment irrespective of pathology and then studied the specific impact of amyloid pathology. After detailed clinical and neuropsychological characterization as well as a positron emission tomography (PET) scans with the tracer 11-[C]-Pittsburgh Compound B to estimate cerebral amyloid deposition, 14 subjects with mild cognitive impairment (MCI) (mean age 75.6 SD: 8.9) according to standard criteria and 21 cognitively healthy controls (HCS) (mean age 71.8 SD: 4.2) were assessed with EEG-fMRI. Thalamo-cortical alpha-fMRI signal coupling was only observed in HCS. Additional EEG-fMRI signal coupling differences between HCS and MCI were observed in parts of the default mode network, salience network, fronto-parietal network, and thalamus. Individuals with significant cerebral amyloid deposition (amyloid-positive MCI and HCS combined compared to amyloid-negative HCS) displayed abnormal EEG-fMRI signal coupling in visual, fronto-parietal regions but also in the parahippocampus, brain stem, and cerebellum. This finding was paralleled by stronger absolute fMRI signal in the parahippocampus and weaker absolute fMRI signal in the inferior frontal gyrus in amyloid-positive subjects. We conclude that the thalamocortical coupling in the alpha band in HCS more closely reflects previous findings observed in younger adults, while in MCI there is a clearly aberrant coupling in several networks dominated by an anticorrelation in the posterior cingulate cortex. While these findings may broadly indicate physiological changes in MCI, amyloid pathology was specifically associated with abnormal fMRI signal responses and disrupted coupling between brain oscillations and fMRI signal responses, which especially involve core regions of memory: the hippocampus, para-hippocampus, and lateral prefrontal cortex.


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