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Related Concept Videos

Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

Indirect-Acting Cholinergic Agonists: Mechanism of Action

Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex, leading to...
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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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Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

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Amyloid Fibrils03:03

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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. 
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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...

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Related Experiment Video

Updated: Jul 6, 2026

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

Potent beta-amyloid modulators.

E García-Palomero1, P Muñoz, P Usan

  • 1Neuropharma SA, Madrid, Spain.

Neuro-Degenerative Diseases
|March 7, 2008
PubMed
Summary
This summary is machine-generated.

Dual binding site acetylcholinesterase (AChE) inhibitors show promise for Alzheimer's disease (AD). NP-61 reversed cognitive impairment and reduced amyloid plaques in mice, suggesting a disease-modifying therapy.

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Published on: January 25, 2018

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is characterized by beta-amyloid plaques.
  • Acetylcholinesterase (AChE) is a drugable target for AD.
  • Dual binding site AChE inhibitors may modify AD pathology.

Purpose of the Study:

  • To identify potent dual binding site AChE inhibitors.
  • To evaluate NP-61 as a potential disease-modifying agent for AD.

Main Methods:

  • Synthesis of novel AChE inhibitor families.
  • In vitro assessment of AChE inhibition and beta-amyloid aggregation.
  • In vivo evaluation of NP-61 in transgenic AD mice (Morris water maze, plaque load analysis).

Main Results:

  • Several drug candidates exhibited subnanomolar AChE inhibition and low micromolar anti-amyloid activity.
  • NP-61 treatment reversed cognitive deficits in AD mice.
  • NP-61 reduced brain amyloid plaque load in AD mice.

Conclusions:

  • NP-61 demonstrates potent AChE inhibition and beta-amyloid modulation.
  • NP-61 reverses AD-like neurodegenerative phenotypes in vivo.
  • NP-61 is a promising candidate for clinical development as an AD disease-modifying therapy.