ABSTRACT
A review of the literature on the problem of the use of non-invasive technologies in early diagnosis and prediction of age-associated cognitive decline associated with Alzheimer's disease is presented. The main attention is paid to the study of the buccal epithelium, oral fluid, as surrogate models of degenerative lesions of cerebral structures, as well as determining the role of oral microorganisms in the formation and development of cognitive disorders. An original hypothesis of neurodegenerative lesions of cerebral structures is presented, on the basis of which an algorithm for studying the state of the oral cavity is proposed in order to detect and predict cognitive deficits as early as possible.
Subject(s)
Alzheimer Disease , Cognition Disorders , Cognitive Dysfunction , Alzheimer Disease/diagnosis , Cognition , Cognition Disorders/diagnosis , Cognitive Dysfunction/diagnosis , Cognitive Dysfunction/etiology , Early Diagnosis , Humans , Mouth/pathology , Neuropsychological TestsABSTRACT
The reactivity and functional heterogeneity of cerebral arteries are maintained by the participation of the endothelium in the regulation of the smooth muscles and by the influence of vasoactive peptides upon the neurotransmitter mechanisms. The initial level of the basal tone plays a major role, too.
Subject(s)
Cerebral Arteries/physiology , Animals , Cerebral Arteries/drug effects , Endothelium, Vascular/drug effects , Endothelium, Vascular/physiology , Muscle, Smooth, Vascular/drug effects , Muscle, Smooth, Vascular/physiology , Neurotransmitter Agents/physiology , Vascular Resistance/drug effects , Vascular Resistance/physiology , Vasopressins/pharmacologyABSTRACT
The direct action of atriopeptin on the cell regulation mechanism of the smooth muscle in isolated segments of the portal vein, aorta, pancreatic and cerebral arteries have been studied. It was found that atriopeptin induce the direct relaxation of the smooth muscle in the main vessels only (aorta, portal vein). In the cerebral and pancreatic arteries atriopeptin stops norepinephrine-induced contractions. The data obtained show that the action of the atriopeptin is mediated by Na+-K+ pump activation of smooth muscle cells and restricts vasoconstriction of catecholamine effect.
Subject(s)
Adrenergic Fibers/drug effects , Atrial Natriuretic Factor/pharmacology , Muscle Tonus/drug effects , Muscle, Smooth, Vascular/drug effects , Adrenergic Fibers/physiology , Animals , Drug Interactions , Humans , Muscle Contraction/drug effects , Muscle, Smooth, Vascular/innervation , Muscle, Smooth, Vascular/physiology , Norepinephrine/pharmacology , Strophanthins/pharmacologyABSTRACT
Atriopeptin exerts a direct regulatory vasodilating effect on the mechanism of the regional blood flow maintenance. Under preliminary activation of vascular tone the atrial factor can produce the smooth muscle relaxation. Atriopeptin II is the most active among the three types of atriopeptin, atriopeptin III is the least active.
