ArticleJournal of Alzheimer's disease : JAD2022
Autonomic Dysfunction Impairs Baroreflex Function in an Alzheimer's Disease Animal Model.
Article in Journal of Alzheimer's disease : JAD, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Blunted pressor response to peripheral sensory afferent nerve stimulation in intracerebroventricular-streptozotocin injected rats.Autonomic neuroscience : basic & clinical · 2025Article
- Glutamate stress in the caudal nucleus tractus solitarii (nTS): Impact on respiratory function and synaptic signaling in an Alzheimer's disease model.Experimental neurology · 2025Article
- The pathophysiology of mixed Alzheimer's disease and vascular dementia.Theranostics · 2025Review
- Synaptic loss and gliosis in the nucleus tractus solitarii with streptozotocin-induced Alzheimer's disease.Brain research · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlzheimer's disease (AD) patients frequently present with orthostatic hypotension. This inability to reflexively increase blood pressure on standing is a serious health concern and increases the risk of stroke and cardiovascular diseases.
objectiveSince there are no clear mechanisms for orthostatic hypotension in human AD, the present study assessed the autonomic changes that could explain this comorbidity in an AD animal model.
methodsWe used the established streptozotocin-induced rat model of AD (STZ-AD), which mimics many hallmark symptoms of sporadic AD in humans. Baroreflex responses were analyzed in anesthetized STZ-AD rats using femoral catheterization for blood pressure and heart rate, and autonomic activity was assessed using specific blockers and splanchnic sympathetic nerve recordings. Expression levels of autonomic receptors at the heart were examined using the western blot technique.
resultsBaroreflex function in STZ-AD showed a blunted heart rate (HR) response to low blood pressure challenges, and the maximal sympathetic nerve activity was reduced. Conversely, HR responses to high blood pressure were similar to control, indicating no change in parasympathetic nerve activity. Under resting conditions, autonomic blockade demonstrated a baseline shift to increased sympathetic tone in STZ-AD. Protein expression levels of beta-1 adrenergic receptor and muscarinic acetylcholine receptor M2 in the heart were unchanged.
conclusionOur study provides the first data on the pathological influence of AD on baroreflex function, which primarily affected the sympathetic nervous system in STZ-AD. These results represent the first mechanisms that may correlate with the orthostatic hypotension in human AD.
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