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Alzheimer's Disease: Treatment

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...

Amyloid Fibrils

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...

Amyloid Fibrils

Amyloid Fibrils

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Related Experiment Video

Updated: Mar 29, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

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Published on: July 14, 2010

2,3,4-Trihydroxybenzophenone Disassembles Amyloid β Aggregates and Ameliorates Synaptic Deficits.

Eunbi Cho^1,2, Kumju Youn³, Huiyoung Kwon⁴

¹Department of Pharmacology, College of Medicine, Konkuk University, Chungju 27478, Republic of Korea.

|March 28, 2026

Summary

2,3,4-trihydroxybenzophenone (THB) effectively inhibits amyloid-beta (Aβ) aggregation and reduces pathology in Alzheimer

Keywords:

2,3,4-tetrahydrobenzophenone 5XFAD Alzheimer’s disease aggregation amyloid β synaptic plasticity

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Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

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Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

Alzheimer's disease (AD) lacks disease-modifying therapies.
Current amyloid-beta (Aβ)-targeting antibodies have limitations.
Small molecules reducing toxic Aβ aggregates are needed.

Purpose of the Study:

Investigate 2,3,4-trihydroxybenzophenone (THB) effects on Aβ₁-42 aggregation and disassembly.
Assess THB's neuroprotective and synaptic function effects in vitro and in vivo.

Main Methods:

In vitro assays for Aβ₁-42 aggregation and fibril disassembly.
Cell viability and hippocampal slice electrophysiology.
In vivo studies in Aβ₁-42 injected and 5XFAD mice (behavioral, histological, electrophysiological analyses).

Main Results:

THB inhibited Aβ₁-42 aggregation and disassembled preformed fibrils.
THB reduced Aβ₁-42-induced cell death and restored synaptic plasticity.
THB decreased amyloid pathology, neuroinflammation, and improved memory in mouse models.

Conclusions:

THB modulates pathogenic Aβ₁-42 assemblies.
THB shows potential for Alzheimer's disease prevention or modification.
Provides a basis for developing small-molecule Aβ modulators.