2-(4--(methylamino)phenyl)-6-hydroxybenzothiazole and Sleep-Apnea--Obstructive

The suggested association between severe obstructive sleep apnea (OSA) and risk of Alzheimer's disease (AD) needs further study. Only few recent reports exist on associations between brain amyloid-β (Aβ) burden and severe OSA in middle-aged patients.. Examine the possible presence of cortical Aβ accumulation in middle-aged patients with severe OSA.. We performed detailed multimodal neuroimaging in 19 cognitive intact patients (mean 44.2 years) with severe OSA (Apnea-Hypopnea Index >30 h-1). Known etiological factors for possible Aβ accumulation were used as exclusion criteria. Aβ uptake was studied with [11C]-PiB-PET, glucose metabolism with [18F]-FDG-PET, and structural imaging with 3.0T MRI.. When analyzed individually, in [11C]-PiB-PET a substantial number (∼32%) of the patients exhibited statistically significant evidence of increased cortical Aβ uptake based on elevated regional Z-score values, mostly seen bilaterally in the precuneus and posterior cingulum regions. Cortical glucose hypometabolism in [18F]-FDG-PET was seen in two patients. MRI did not show structural changes suggestive of AD-related pathology.. Increased [11C]-PiB uptake was seen in middle-aged cognitively intact patients with severe OSA. These findings are similar to those described in cognitive unimpaired older OSA patients. The changes in cortical Aβ uptake suggest that severe OSA itself may predispose to alterations related to AD already in middle-age. Aβ clearance may be compromised without simultaneous evidence of metabolic or structural alterations. The results emphasize the importance of early diagnostics and proper treatment of severe OSA in cognitively intact middle-aged subjects, possibly diminishing the individual risk for later cognitive dysfunction.

Topics: Adult; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Cerebral Cortex; Female; Fluorodeoxyglucose F18; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Radiopharmaceuticals; Severity of Illness Index; Sleep Apnea, Obstructive; Thiazoles

Disturbed sleep due to obstructive sleep apnea syndrome (OSAS) might accelerate amyloidβ (Aβ) deposition, which can be a crucial factor in Alzheimer's disease. We studied Aβ deposition in untreated OSAS patients with normal cognition.. The abnormal accumulation of enhanced. The OSAS severity alone may not predict Aβ deposition in OSAS patients with normal cognition.

Topics: Aged; Aged, 80 and over; Amyloid; Aniline Compounds; Brain; Cognition; Female; Humans; Male; Middle Aged; Positron Emission Tomography Computed Tomography; Sleep Apnea, Obstructive; Thiazoles

To test the hypothesis that excessive amyloid deposition is a biological link between obstructive sleep apnea (OSA) and Alzheimer's disease, we determined whether OSA increases cerebral amyloid burden, relative to controls, using Pittsburgh Compound B (PiB) PET imaging. The subjects were adult participants (age 50-65 years) from the Korean Genome and Epidemiology Study. Polysomnography, brain MRI including 3D images, and a detailed neuro-cognitive function test battery were done in 2011-2012. Nineteen OSA subjects (Apnea-Hypopnea Index [AHI] ≥15/h, 21.2±5.1/h; age 58.5±4.1 years; 9 male) and 19 controls (AHI 1.8±1.3/h; age 58.5±4.2 years; 9 male) underwent 60-min dynamic 11C-PiB PET. All subjects were right-handed with normal cognitive function and brain MRI. Controls were matched by age, gender, education, and APOE genotype. A voxel-wise comparison of PiB-PET images between the two groups was performed after spatial and count normalization with cerebellar gray matter as a reference. Covariates included the status of sleep duration, hypertension, diabetes, body mass index, exercise, depressive mood, smoking, and alcohol drinking. Cortical thickness on 3D MRI was also measured and compared between the two groups. The OSA group showed a higher PiB deposition in the right posterior cingulate gyrus and right temporal cortex (corrected p < 0.05). There was no area of higher uptake in the control compared with OSA. Regional differences in cortical thickness were not significant. The study suggests that OSA accelerates amyloid deposition and may contribute to the development or progression of Alzheimer's disease.

Topics: Aged; Amyloid; Aniline Compounds; Apolipoproteins E; Brain; Carbon Radioisotopes; Cohort Studies; Female; Humans; Independent Living; Male; Middle Aged; Neuropsychological Tests; Polysomnography; Positron-Emission Tomography; Republic of Korea; Sleep Apnea, Obstructive; Thiazoles