2022
DOI: 10.1590/0004-282x-anp-2021-0147
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Medication reconciliation role and value in Alzheimer's disease treatment

Abstract: Background: With the continuous increase of Alzheimer's disease (AD), it is also imminent to treat patients with AD for medication reconciliation. Objective: To explore the role and value of medication reconciliation in AD treatment. Methods: 100 patients over 65 years of age diagnosed with AD were randomly separated into two groups: conventional treatment and medication reforming. The list of medical orders of all subjects was obtained within 24 hours after admission with Beers criteria, STOPP/START criteri… Show more

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“…As the main active components of ginseng , ginsenosides feature antitumor, anti-inflammatory, antioxidant, and antiapoptotic effects [ 12 ]. Ginseng protein is one of the active components of ginseng with anti-AD effects in vivo and in vitro [ 13 , 14 ], and the mechanism of action is associated with the activation of the cyclic adenosine monophosphate/cyclic phosphoadenosine effector element-binding protein (cAMP/CREB) signaling pathway. Brain-derived neurotrophic factor (BDNF) is a CREB downstream effector that binds to tyrosine-protein kinase receptor B (TrkB), causing an increase in TrkB autophosphorylation, which consequently facilitates neuronal growth, survival, and differentiation [ 15 , 16 ] and protects against neuronal damage elicited by β -amyloid (A β ) [ 17 ].…”
Section: Introductionmentioning
confidence: 99%
“…As the main active components of ginseng , ginsenosides feature antitumor, anti-inflammatory, antioxidant, and antiapoptotic effects [ 12 ]. Ginseng protein is one of the active components of ginseng with anti-AD effects in vivo and in vitro [ 13 , 14 ], and the mechanism of action is associated with the activation of the cyclic adenosine monophosphate/cyclic phosphoadenosine effector element-binding protein (cAMP/CREB) signaling pathway. Brain-derived neurotrophic factor (BDNF) is a CREB downstream effector that binds to tyrosine-protein kinase receptor B (TrkB), causing an increase in TrkB autophosphorylation, which consequently facilitates neuronal growth, survival, and differentiation [ 15 , 16 ] and protects against neuronal damage elicited by β -amyloid (A β ) [ 17 ].…”
Section: Introductionmentioning
confidence: 99%