Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly. A Longitudinal Study

Obstructive sleep apnea treatment, slow wave activity, and amyloid‐β

“…20 Given the high prevalence of OSA, if the effects on Aβ could be mitigated with treatment, improving OSA diagnosis and treatment could potentially reduce AD risk on a broad scale. The effect of OSA on SWA and Aβ-and possibly tauis a probable proximal step in a cascade whereby OSA increases the risk of AD.…”

Gray matter volume and estimated brain age gap are not associated with sleep-disordered breathing in subjects from the ADNI cohort

“…This is indicative that despite the frequent clinical co-occurrence of SDB and AD, there may be no synergy between them in accelerating gray matter atrophy. Recent investigations using cerebrospinal fluid and PET imaging suggest an interplay between amyloid production/clearance and SDB 17,42,56–58 . These include an impairment in the cerebrospinal fluid-interstitial fluid exchange 60 , cerebral edema secondary to an intermittent hypoxia 61 (similar to the increase in brain volume and pseudoatrophy observed in multiple sclerosis), and compensatory excessive neuronal synaptic activity 62 in SDB, all of which could potentially lead to an increase in beta-amyloid deposition and its clearance reduction.…”

“…These include an impairment in the cerebrospinal fluid-interstitial fluid exchange 60 , cerebral edema secondary to an intermittent hypoxia 61 (similar to the increase in brain volume and pseudoatrophy observed in multiple sclerosis), and compensatory excessive neuronal synaptic activity 62 in SDB, all of which could potentially lead to an increase in beta-amyloid deposition and its clearance reduction. It is therefore possible that the presence of SDB is associated with AD risk only through beta-amyloid deposition 42,58 or altered brain function 63–65 , but an interaction should have been observed in MCI or AD where it is generally accepted that neuronal loss follows amyloid deposition. More studies are needed to better understand the compensatory increase in gray matter volume in SDB suggested by several studies, as well as the precise progression of brain atrophy in AD, as both may have contributed to obtaining such negative findings.…”

The transition from vivid dreams over floccillations and visual hallucinations to complete delirium in a geriatric patient at the dawn of Alzheimer's dementia: beneficial role of rivastigmine

“…The impact of OSA on the generation of these biomarkers is under study as severe OSA may increase the risk of developing AD (resp. brain amyloid burden) and, moreover, intermittent hypoxia/re‐oxygenation was demonstrated to increase extra‐ and intracellular levels of beta‐amyloid in mice brains . Such proteins were strongly related to subsequently progressing CCD which promotes cognitive deficits including disturbed sleep‐wake cycle as well as reduced vigilance, alertness, attention and memory in patients with AD, delirium and the interface of both .…”