stilbenes and Atrophy

Neocortical atrophy reduces PET signal intensity, potentially affecting the diagnostic efficacy of β-amyloid (Aβ) brain PET imaging. This study investigated whether partial-volume effect correction (PVEC), adjusting for this atrophy bias, improves the accuracy of (18)F-florbetaben Aβ PET.. We analyzed (18)F-florbetaben PET and MRI data obtained from 3 cohorts. The first was 10 patients with probable Alzheimer disease (AD) and 10 age-matched healthy controls (HCs), the second was 31 subjects who underwent in vivo imaging and postmortem histopathology for Aβ plaques, and the third was 5 subjects who underwent PET and MRI at baseline and 1 y later. The imaging data were coregistered and segmented. PVEC was performed using the voxel-based modified Müller-Gärtner method (PVELab, SPM8). From the PET data, regional and composite SUV ratios (SUVRs) with and without PVEC were obtained. In the MRI data, mesial temporal lobe atrophy was determined by the Scheltens mesial temporal atrophy scale and gray matter volumes by voxel-based morphometry.. In cohort 1, PVEC increased the effect on AD-versus-HC discrimination from a Cohen d value of 1.68 to 2.0 for composite SUVRs and from 0.04 to 1.04 for mesial temporal cortex SUVRs. The PVEC-related increase in mesial temporal cortex SUVR correlated with the Scheltens score (r = 0.84, P < 0.001), and that of composite SUVR correlated with the composite gray matter volume (r = -0.75, P < 0.001). In cohort 2, PVEC increased the correlation coefficient between mesial temporal cortex SUVR and histopathology score for Aβ plaque load from 0.28 (P = 0.09) to 0.37 (P = 0.03). In cohort 3, PVEC did not affect the composite SUVR dynamics over time for the Aβ-negative subject. This finding was in contrast to the 4 Aβ-positive subjects, in 2 of whom PVEC changed the composite SUVR dynamics.. The influence of PVEC on (18)F-florbetaben PET data is associated with the degree of brain atrophy. Thus, PVEC increases the ability of (18)F-florbetaben PET to discriminate between AD patients and HCs, to detect Aβ plaques in the atrophic mesial temporal cortex, and potentially to evaluate changes in brain Aβ load over time. As such, the use of PVEC should be considered for quantitative (18)F-florbetaben PET scans, especially in assessing patients with brain atrophy.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Atrophy; Cerebral Cortex; Cohort Studies; Female; Humans; Image Processing, Computer-Assisted; Longitudinal Studies; Magnetic Resonance Imaging; Male; Plaque, Amyloid; Positron-Emission Tomography; Radiopharmaceuticals; Stilbenes; Temporal Lobe

To investigate the topographical distribution of tau pathology and its effect on functional and structural changes in patients with Alzheimer disease (AD) and mild cognitive impairment (MCI) by using (18)F-AV-1451 PET.. We included 20 patients with AD, 15 patients with MCI, and 20 healthy controls, and performed neuropsychological function tests, MRI, as well as (18)F-florbetaben (for amyloid) and (18)F-AV-1451 (for tau) PET scans. By using the regional volume-of-interest masks extracted from MRIs, regional binding values of standardized uptake value ratios and volumes were measured. We compared regional binding values among 3 diagnostic groups and identified correlations among the regional binding values, performance in each cognitive function test, and regional atrophy.. (18)F-AV-1451 binding was increased only in the entorhinal cortex in patients with MCI, while patients with AD exhibited greater binding in most cortical regions. In the 35 patients with MCI and AD, (18)F-AV-1451 binding in most of the neocortex increased with a worsening of global cognitive function. The visual and verbal memory functions were associated with the extent of (18)F-AV-1451 binding, especially in the medial temporal regions. The (18)F-AV-1451 binding also correlated with the severity of regional atrophy of the cerebral cortex.. Tau PET imaging with (18)F-AV-1451 could serve as an in vivo biomarker for the evaluation of AD-related tau pathology and monitoring disease progression. The accumulation of pathologic tau is more closely related to functional and structural deterioration in the AD spectrum than β-amyloid.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Atrophy; Cognitive Dysfunction; Disease Progression; Entorhinal Cortex; Female; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging; Male; Memory; Neuropsychological Tests; Positron-Emission Tomography; Prospective Studies; Radiopharmaceuticals; Stilbenes; tau Proteins; Vision, Ocular

The "fetal basis of adult disease" hypothesis proposes that prenatal exposure to environmental stress can lead to increased susceptibility to clinical disorders later in life. In utero exposure of fetus to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to alterations in T-cell differentiation in the thymus and increased susceptibility to autoimmune disease later in life. TCDD triggers toxicity through activation of aryl hydrocarbon receptor and severely affects maternal and fetal immune system during pregnancy.. In this study, using a mouse model, we investigated if administration of resveratrol (RES; 3,5,4'-trihydroxystilbene) would inhibit immunotoxicity induced by TCDD during pregnancy in the mother and fetus. We observed that RES protected not only normal nonpregnant mice but also pregnant mothers and their fetuses from TCDD-induced thymic atrophy, apoptosis, and alterations in the expression of T-cell receptor and costimulatory molecules as well as T-cell differentiation. In addition, there was significantly reduced expression of CYP1A1 in thymi of both the mother and the fetus when RES was used in vivo post-TCDD exposure.. In conclusion, these studies demonstrate that consumption of RES, a natural plant product, during pregnancy, may afford protection to the mother and the fetus from the toxicity induced by environmental pollutants that mediate their effects through activation of aryl hydrocarbon receptor.

Topics: Animals; Apoptosis; Atrophy; Cell Differentiation; Cells, Cultured; Cytochrome P-450 CYP1A1; Environmental Pollutants; Female; Fetus; Gene Expression Regulation; Maternal Exposure; Mice; Mice, Inbred C57BL; Polychlorinated Dibenzodioxins; Pregnancy; Protective Agents; Receptors, Aryl Hydrocarbon; Resveratrol; Stilbenes; T-Lymphocyte Subsets; Thymus Gland

Neuroimaging evidence showed structural and/or functional abnormalities existing in the central nervous system, especially the hippocampus, in chronic fatigue syndrome (CFS) patients. However, its pathophysiologic mechanisms are unclear in part due to the lack of an applicable animal model. We established a chronic fatigue murine model by six repeated injections of Brucella abortus antigen to mice, which was manifested as reduced daily running activity and hippocampal atrophy. Thereafter, resveratrol, a polyphenolic activator of sirtuin 1, was used for treatment in this model. Daily running activity was increased by more than 20%, and the hippocampus was enlarged after 4-week resveratrol therapy. Furthermore, resveratrol inhibited neuronal apoptosis and expression of hippocampal acetylated p53 in the fatigue mice. Resveratrol also improved neurogenesis and expression of brain-derived neurotrophic factor mRNA in the hippocampus. We concluded that repeated injection of B. abortus antigen could induce hypoactivity and hippocampal atrophy in mice. Resveratrol may be effective for improving fatigue symptoms and enlarging the atrophic hippocampus by repressing apoptosis and promoting neurogenesis.

Topics: Animals; Apoptosis; Atrophy; Brain-Derived Neurotrophic Factor; Brucella abortus; Disease Models, Animal; Fatigue Syndrome, Chronic; Female; Hippocampus; Mice; Mice, Inbred BALB C; Neurogenesis; Neurons; Neuroprotective Agents; Phytotherapy; Plant Extracts; Resveratrol; RNA, Messenger; Stilbenes

Topics: 17-Ketosteroids; Adenocarcinoma; Atrophy; Chorionic Gonadotropin; Clomiphene; Diagnosis; Drug Therapy; Endometriosis; Endometrium; Female; Follicle Stimulating Hormone; Genital Diseases, Female; Gonadotropins; Humans; Hyperplasia; Infertility; Infertility, Female; Ovulation; Pathology; Polycystic Ovary Syndrome; Stilbenes; Toxicology; Urine; Uterine Neoplasms