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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 ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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...
Amyloid Fibrils03:03

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, normally used to...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

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Related Experiment Video

Updated: Jun 2, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

Neuroprotective Phytochemicals Targeting Amyloid and Tau Pathologies.

Irfan Ahmed1, Yaasir Ahmed Ansari2, Gazala Parveen3

  • 1Regional Research Institute of Unani Medicine, Mumbai, 400008, M.S., India.

Current Topics in Medicinal Chemistry
|June 1, 2026
PubMed
Summary

Phytochemicals show promise in treating Alzheimer's disease by targeting both amyloid and tau pathologies. Further research into delivery methods is needed for clinical application of these multi-target therapies.

Keywords:
Alzheimer's diseaseAmyloid-betaFlavonoidsNatural products.NeuroprotectionPhytochemicalsTau hyperphosphorylation

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A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Related Experiment Videos

Last Updated: Jun 2, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease affects over 55 million globally, projected to reach 152 million by 2050.
  • Current treatments are largely symptomatic, failing to address core molecular issues like oxidative stress, mitochondrial dysfunction, and neuroinflammation.
  • Neurodegeneration in Alzheimer's involves complex pathways converging on amyloid-beta (Aβ) and hyperphosphorylated Tau.

Purpose of the Study:

  • To review phytochemicals with dual anti-amyloid and anti-tau effects, addressing multiple Alzheimer's pathologies simultaneously.
  • To assess over 100 bioactive compounds from 7 chemical families for their potential in Alzheimer's disease therapy.
  • To identify therapeutic strategies that move beyond single-target approaches for Alzheimer's disease.

Main Methods:

  • Comprehensive literature review of PubMed, Scopus, and Web of Science databases up to 2025.
  • Analysis of phytochemicals targeting both amyloid and tau pathologies.
  • Evaluation of compounds based on their effects on key molecular pathways and preclinical model outcomes.

Main Results:

  • Identified major phytochemicals (e.g., curcumin, resveratrol, EGCG) with dual anti-amyloid and anti-tau activity.
  • These compounds inhibit beta-secretase, prevent amyloid fibril formation, reduce Tau phosphorylation, and enhance cellular clearance mechanisms.
  • Phytochemicals modulate Nrf2 and NF-κB pathways, reducing oxidative stress and neuroinflammation.
  • Preclinical studies show cognitive and neuropathological improvements, but bioavailability and blood-brain barrier penetration remain challenges.

Conclusions:

  • Phytochemicals offer a multi-target therapeutic strategy for Alzheimer's disease, addressing its complex molecular underpinnings.
  • Nanotechnology and structural modifications show potential for overcoming pharmacokinetic limitations.
  • These findings suggest a paradigm shift towards disease-modifying therapies for Alzheimer's, moving beyond symptomatic management.