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Related Concept Videos

Alzheimer's Disease: Treatment01:22

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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 (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: Feb 23, 2026

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections
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Changes in brain amyloid-β accumulation after donepezil administration.

Kenji Ishibashi1, Yoshiharu Miura2, Kei Wagatsuma3

  • 1Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan; Department of Neurology, Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital, Tokyo, Japan.

Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia
|September 3, 2017
PubMed
Summary

Donepezil treatment did not reduce amyloid-β (Aβ) accumulation in Alzheimer's disease (AD) patients over one year. Brain Aβ levels increased despite donepezil administration, contrary to findings in mouse models.

Keywords:
(11)C-PiBAlzheimer’s diseaseAmyloidDonepezilPET

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Area of Science:

  • Neurology
  • Neuroscience
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) plaque accumulation in the brain.
  • Donepezil, an acetylcholinesterase inhibitor, has shown promise in reducing Aβ in mouse models of AD.

Purpose of the Study:

  • To investigate the efficacy of donepezil in reducing brain Aβ accumulation in human patients with Alzheimer's disease.
  • To determine if one year of donepezil treatment alters Aβ burden in AD patients.

Main Methods:

  • Ten AD patients underwent two 11C-Pittsburgh Compound B (PiB) PET scans approximately one year apart.
  • Standardized uptake value ratio (SUVR) was calculated in Aβ-preferred regions, using the cerebellum as a reference.
  • Patients received either 5mg or 10mg of donepezil daily.

Main Results:

  • A significant increase in SUVR was observed between the first and second PET sessions (P=0.026).
  • This indicates a higher brain Aβ accumulation after one year of donepezil treatment.
  • The findings contradict previous results from mouse models.

Conclusions:

  • One year of donepezil administration does not reduce, and may even increase, brain Aβ accumulation in human patients with Alzheimer's disease.
  • Donepezil's efficacy in reducing Aβ burden may not translate from mouse models to human AD patients.
  • Further research is needed to understand donepezil's long-term effects on Aβ pathology in humans.