The associations of inflammation/immune responses with clinical presentations of Alzheimer’s disease (AD) remain unclear. We hypothesized that TNF-α and elevated antibodies to periodontal bacteria would be greater in AD compared to normal controls (NL) and their combination would aid clinical diagnosis of AD. Plasma TNF-α and antibodies against periodontal bacteria were elevated in AD patients compared with NL and independently associated with AD. The number of positive IgG to periodontal bacteria incremented the TNF-α classification of clinical AD and NL. This study shows that TNF-α and elevated numbers of antibodies against periodontal bacteria associate with AD and contribute to the AD diagnosis.
We previously showed that upper airway resistance can be inferred from the inspiratory flow contour during continuous positive airway pressure (CPAP) titration in obstructive sleep apnea syndrome (OSAS). The present study examines whether similar information can be obtained from inspiratory flow measured by a nasal cannula/pressure transducer. Ten symptomatic patients (snoring, upper airway resistance syndrome [UARS], or OSAS) and four asymptomatic subjects underwent nocturnal polysomnography (NPSG) with monitoring of flow (nasal cannula) and respiratory driving pressure (esophageal or supraglottic catheter). For each breath the inspiratory flow signal was classified as normal, flattened, or intermediate by custom software. "Resistance" was calculated from peak inspiratory flow and pressure, and normalized to the resistance during quiet wakefulness. Resistance in all stages of sleep was increased for breaths with flattened (387 +/- 188%) or intermediate (292 +/- 163%) flow contour. In combination with apnea-hypopnea index (AHI), identification of "respiratory events," consisting of consecutive breaths with a flattened contour, allowed differentiation of symptomatic from asymptomatic subjects. Our data show that development of a plateau on the inspiratory flow signal from a nasal cannula identifies increased upper airway resistance and the presence of flow limitation. In patients with symptoms of excessive daytime somnolence and low AHI this may help diagnose the UARS and separate it from nonrespiratory causes of sleep fragmentation.
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