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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
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Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...

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Related Experiment Video

Updated: May 22, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
11:13

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration

Published on: June 9, 2023

Salidroside mitigates cognitive deficits in AlCl3 exposed aging mouse by modulating APP processing and mitochondrial

Yiru Dong1, Huiling Jin1, Shengmin Wang1

  • 1Neurotoxicology Laboratory, Department of Preventive Medicine, Yanbian University, Yanji, Jilin, China.

Frontiers in Behavioral Neuroscience
|May 21, 2026
PubMed
Summary
This summary is machine-generated.

Salidroside, derived from Rhodiola rosea, shows promise in treating Alzheimer's disease by improving cognitive function and reducing amyloid-beta. It protects mitochondria and balances redox in both animal models and cell cultures.

Keywords:
APP processingAlzheimer’s diseaseamyloid-betamitochondrial dysfunctionsalidroside

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Analysis of Learning and Memory Ability in an Alzheimer's Disease Mouse Model using the Morris Water Maze
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Analysis of Learning and Memory Ability in an Alzheimer's Disease Mouse Model using the Morris Water Maze
07:07

Analysis of Learning and Memory Ability in an Alzheimer's Disease Mouse Model using the Morris Water Maze

Published on: October 29, 2019

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Mitochondrial dysfunction and oxidative stress are central to Alzheimer's disease (AD) progression.
  • Salidroside, a Rhodiola rosea extract, has known neuroprotective and antioxidant effects.
  • Its specific impact on AD-related mitochondrial issues and amyloid precursor protein (APP) processing requires further study.

Purpose of the Study:

  • To investigate the neuroprotective effects of salidroside on Alzheimer's disease models.
  • To assess salidroside's influence on mitochondrial function and APP processing in AD.
  • To evaluate salidroside's potential therapeutic benefits for cognitive deficits.

Main Methods:

  • Utilized both in vivo (AlCl3-induced aging mouse model) and in vitro (HT-22 hippocampal neurons) experimental setups.
  • Assessed behavioral changes, brain biomarkers, mitochondrial function, oxidative stress, apoptosis, and APP processing.
  • Administered salidroside to evaluate its impact on AD-related pathologies.

Main Results:

  • Salidroside improved cognitive performance and reduced amyloid-beta (Aβ) deposition in mice by modulating APP processing (downregulating β- and γ-secretase, upregulating α-secretase).
  • Observed decreased mitochondrial protein aggregation and restored mitochondrial function and redox balance in treated mice.
  • In vitro, salidroside reduced reactive oxygen species (ROS), inhibited neuronal apoptosis, and suppressed Aβ production.

Conclusions:

  • Salidroside may mitigate mitochondrial dysfunction and protein aggregation by influencing APP processing, boosting sAPPα, and reducing Aβ.
  • These findings suggest salidroside's potential in treating mitochondrial impairment and cognitive deficits in Alzheimer's disease.
  • Further research is warranted to confirm salidroside's therapeutic efficacy for AD.