Tau PET Distributional Pattern in AD Patients with Visuospatial Dysfunction
Xi SunBinbin NieShujun ZhaoQian ChenPanlong LiTianhao ZhangTingting PanTing FengLuying WangXiaolong YinWei ZhangShilun ZhaoBaoci ShanHua LiuShengxiang LiangLin AiGuihong Wang
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Abstract:
Visuospatial dysfunction is one predominant symptom in many atypical Alzheimer's disease (AD) patients, however, until now its neural correlates still remain unclear. For the accumulation of intracellular hyperphosphorylated tau proteins is a major pathogenic factor in neurodegeneration of AD, the distributional pattern of tau could highlight the affected brain regions associated with specific cognitive deficits.We investigated the brain regions particularly affected by tau accumulation in patients with visuospatial dysfunction to explore its neural correlates.Using 18F-AV-1451 tau positron emission tomography (PET), voxel-wise two-sample t-tests were performed between AD patients with obvious visuospatial dysfunction (VS-AD) and cognitively normal subjects, AD patients with little-to-no visuospatial dysfunction (non VS-AD) and cognitively normal subjects, respectively.Results showed increased tau accumulations mainly located in occipitoparietal cortex, posterior cingulate cortex, precuneus, inferior and medial temporal cortex in VS-AD patients, while increased tau accumulations mainly occurred in the inferior and medial temporal cortex in non VS-AD patients.These findings suggested that occipitoparietal cortex, posterior cingulate cortex and precuneus, which were particularly affected by increased tau accumulation in VS-AD patients, may associate with visuospatial dysfunction of AD.Keywords:
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Dorsolateral prefrontal cortex
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Visuospatial dysfunction is one predominant symptom in many atypical Alzheimer's disease (AD) patients, however, until now its neural correlates still remain unclear. For the accumulation of intracellular hyperphosphorylated tau proteins is a major pathogenic factor in neurodegeneration of AD, the distributional pattern of tau could highlight the affected brain regions associated with specific cognitive deficits.We investigated the brain regions particularly affected by tau accumulation in patients with visuospatial dysfunction to explore its neural correlates.Using 18F-AV-1451 tau positron emission tomography (PET), voxel-wise two-sample t-tests were performed between AD patients with obvious visuospatial dysfunction (VS-AD) and cognitively normal subjects, AD patients with little-to-no visuospatial dysfunction (non VS-AD) and cognitively normal subjects, respectively.Results showed increased tau accumulations mainly located in occipitoparietal cortex, posterior cingulate cortex, precuneus, inferior and medial temporal cortex in VS-AD patients, while increased tau accumulations mainly occurred in the inferior and medial temporal cortex in non VS-AD patients.These findings suggested that occipitoparietal cortex, posterior cingulate cortex and precuneus, which were particularly affected by increased tau accumulation in VS-AD patients, may associate with visuospatial dysfunction of AD.
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Background: Cognitive frailty and impairment are phenotypically and pathophysiologically correlated with physical frailty. We examined associations between accumulation of amyloid-β in the brain as a brain imaging biomarker and phenotypes of physical frailty (weight loss, weakness, exhaustion, slowness, low physical activity) in older adults with mild cognitive impairment (MCI) and cognitive frailty. Methods: Cross-sectional associations between brain amyloid-β accumulation measured with 11C-Pittsburgh compound B (PiB)-positron emission tomography (PET) and physical frailty were examined in 48 elderly participants (mean age: 75.1 ± 6.6 years; 73% female). Cortical and regional standard uptake value ratios (SUVRs) were obtained. Main outcome measures included frailty phenotypes and physical functions (gait speed, short physical performance battery, and Timed Up and Go tests). Results: Mean cortical region of interest and regional SUVRs (frontal cortex, temporal cortex, parietal cortex, precuneus/posterior cingulate cortex (PC/PCC), hippocampus, basal ganglia, and global SUVR) were associated with gait speed, Timed Up and Go, and short physical performance battery (PC/PCC, basal ganglia). In addition, SUVRs of all brain regions were significantly linked to weakness. Conclusion: SUVRs of all brain regions revealed an association between brain amyloid-β accumulation and weakness. Furthermore, global SUVRs (frontal cortex, temporal cortex, parietal cortex, PC/PCC, hippocampus, basal ganglia) were associated with gait parameters.
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BACKGROUND AND PURPOSE:
High-altitude environmental factors and genetic variants together could have exerted their effects on the human brain. The present study was designed to investigate the cerebral morphology in high-altitude native Tibetans.MATERIALS AND METHODS:
T1-weighted brain images were obtained from 77 Tibetan adolescents on the Qinghai-Tibetan Plateau (altitude, 2300–5300 m) and 80 matched Han controls living at sea level. Cortical thickness, curvature, and sulcus were analyzed by using FreeSurfer.RESULTS:
Cortical thickness was significantly decreased in the left posterior cingulate cortex, lingual gyrus, superior parietal cortex, precuneus, and rostral middle frontal cortex and the right medial orbitofrontal cortex, lateral occipital cortex, precuneus, and paracentral lobule. Curvature was significantly decreased in the left superior parietal cortex and right superior marginal gyrus; the depth of the sulcus was significantly increased in the left inferior temporal gyrus and significantly decreased in the right superior marginal gyrus, superior temporal gyrus, and insular cortex. Moreover, cortical thickness was negatively correlated with altitude in the left superior and middle temporal gyri, rostral middle frontal cortex, insular cortex, posterior cingulate cortex, precuneus, lingual gyrus, and the right superior temporal gyrus. Curvature was positively correlated with altitude in the left rostral middle frontal cortex, insular cortex, and middle temporal gyrus. The depth of the sulcus was negatively correlated with altitude in the left lingual gyrus and right medial orbitofrontal cortex.CONCLUSIONS:
Differences in cortical morphometry in native Tibetans may reflect adaptations related to high altitude.Orbitofrontal cortex
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Abstract This study investigated cerebral glucose metabolism in very early Alzheimer's disease, before a clinical diagnosis of probable Alzheimer's disease is possible, using [ 18 F]fluorodeoxyglucose positron emission tomography. First, 66 patients with probable Alzheimer's disease with a spectrum of dementia severity (Mini‐Mental State Examination score, 0–23) were recruited and studied. Cortical metabolic activity was analyzed topographically using three‐dimensional stereotactic surface projections. Regression analysis was performed for each brain pixel to predict metabolic patterns of very early disease. Predictions were tested prospectively in a group of 8 patients who complained only of memory impairment without general cognitive decline (Mini‐Mental State Examination score, 25 · 1) at the time of scanning but whose condition later progressed to probable Alzheimer's disease. Both results were compared to cerebral metabolic activity in 22 age‐similar normal control subjects. Prediction and analysis of actual patients consistently indicated marked metabolic reduction (21–22%) in the posterior cingulate cortex and cinguloparietal transitional area in patients with very early Alzheimer's disease. Mean metabolic reduction in the posterior cingulate cortex was significantly greater than that in the lateral neocortices or parahippocampal cortex. The result suggests a functional importance for the posterior cingulate cortex in impairment of learning and memory, which is a feature of very early Alzheimer's disease.
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Synaptic loss is a hallmark feature of Alzheimer's disease (AD). Phospholipid metabolism is important for the formation of new and maintenance of existing synapses. It is known that synaptic loss and neurodegeneration follow a distinctive regional pattern during the course of the disease, starting in the hippocampus and progressing to mediotemporal, parietal and frontal regions. To assess whether phospholipid metabolism shows regional variation in AD we performed 3D phosphorus Magnetic Resonance Spectroscopic imaging (31 P-MRSI) of AD patients. 31 P-MRSI is performed as part of a clinical study (NTR3346) in drug-naïve patients with mild AD (MMSE≥20) in which the effect of the medical food Souvenaid ® 1 on brain metabolites is investigated by 31 P-MRS and proton (1 H) MRS. Baseline 31 P-MRS measurements from patients in this study were used in the current analysis to investigate brain phospholipid levels in various brain regions in AD. So far, baseline data of 12 patients have been collected. 31 P-MRSI spectra were acquired of the whole brain at 3T with a dual-tuned 1 H / 31 P volume head coil and a 3D pulse-acquire sequence with the following parameter values: TR=2000 ms, TE=0.10 ms, 40° flip-angle, NA=4, WALTZ4 proton decoupling, nominal voxel size=16x16x16mm). Resonances in spectra from the medial temporal lobe, medial prefrontal cortex and posterior cingulate cortex were fitted, resulting in metabolite levels of the phosphomonoesters phosphocholine (PCho) and phosphoethanolamine (PEtn), and of the phosphodiesters glycerophosphocholine (GPCho) and glycerophosphoethanolamine (GPEtn), inorganic phosphate, phosphocreatine and ATP. High quality 31 P-MRSI spectra with well resolved resonance for phospholipids were obtained (see Figure). Relative levels of PCho, PEtn, GPCho and GPEtn to total phosphorus signal and the ratio of phosphomonoesters to phosphodiesters will be presented for medial temporal lobe, medial prefrontal cortex and posterior cingulate cortex. It is anticipated that data will be presented from a total number of approximately 20 patients.
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Early identification of people at risk of imminent progression to dementia due to Alzheimer disease is crucial for timely intervention and treatment. We investigated whether the texture of MRI brain scans could predict the progression of mild cognitive impairment (MCI) to Alzheimer disease earlier than volume.We constructed a development data set (121 people who were cognitively normal and 145 who had mild Alzheimer disease) and a validation data set (113 patients with stable MCI who did not progress to Alzheimer disease for 3 years; 40 with early MCI who progressed to Alzheimer disease after 12–36 months; and 41 with late MCI who progressed to Alzheimer disease within 12 months) from the Alzheimer’s Disease Neuroimaging Initiative. We analyzed the texture of the hippocampus, precuneus and posterior cingulate cortex using a grey-level co-occurrence matrix. We constructed texture and volume indices from the development data set using logistic regression. Using area under the curve (AUC) of receiver operator characteristics, we compared the accuracy of hippocampal volume, hippocampal texture and the composite texture of the hippocampus, precuneus and posterior cingulate cortex in predicting conversion from MCI to Alzheimer disease in the validation data set.Compared with hippocampal volume, hippocampal texture (0.790 v. 0.739, p = 0.047) and composite texture (0.811 v. 0.739, p = 0.007) showed larger AUCs for conversion to Alzheimer disease from both early and late MCI. Hippocampal texture showed a marginally larger AUC than hippocampal volume in early MCI (0.795 v. 0.726, p = 0.060). Composite texture showed a larger AUC for conversion to Alzheimer disease than hippocampal volume in both early (0.817 v. 0.726, p = 0.027) and late MCI (0.805 v. 0.753, p = 0.019).This study was limited by the absence of histological data, and the pathology reflected by the texture measures remains to be validated.Textures of the hippocampus, precuneus and posterior cingulate cortex predicted conversion from MCI to Alzheimer disease at an earlier time point and with higher accuracy than hippocampal volume.
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