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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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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...
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Alzheimer's Disease: Overview01:26

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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...
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Related Experiment Video

Updated: Dec 25, 2025

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
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Dihydrotanshinone I Increase Amyloid-β Clearance and Decrease Tau Phosphorylation via Enhancing Autophagy.

Zhonglei Bao1, Huixue Zhang1, Hong Jiao1

  • 1Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.

Pharmacology
|March 23, 2020
PubMed
Summary
This summary is machine-generated.

Dihydrotanshinone I (DTS I) enhances autophagy by targeting the AMPK/mTOR pathway, promoting amyloid-β clearance and reducing tau phosphorylation, offering potential Alzheimer

Keywords:
Alzheimer’s diseaseAmyloid-βAutophagyDihydrotanshinone ITau

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) plaques and hyper-phosphorylated tau tangles.
  • Autophagy is a cellular process involved in degrading abnormal substances like Aβ and tau.

Purpose of the Study:

  • To identify novel mammalian target of rapamycin (mTOR) signaling inhibitors.
  • To investigate the effect of dihydrotanshinone I (DTS I) on autophagy and its role in AD pathologies.

Main Methods:

  • Utilized α-Screen assay for inhibitor discovery.
  • Employed laser scanning confocal microscopy to study autophagy.
  • Applied ELISA and Western blot assays to analyze Aβ and tau levels and signaling pathways.

Main Results:

  • Dihydrotanshinone I (DTS I) inhibits mTOR phosphorylation and enhances autophagy by increasing AMPK phosphorylation.
  • DTS I promotes Aβ clearance and decreases tau phosphorylation.
  • The observed effects are mediated through the AMPK/mTOR pathway and autophagy enhancement.

Conclusions:

  • DTS I effectively enhances autophagy via the AMPK/mTOR pathway.
  • DTS I demonstrates therapeutic potential for Alzheimer's disease by clearing Aβ and reducing tau pathology.