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Related Concept Videos

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.
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Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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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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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

Updated: Mar 9, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Oxidative Stress, Synaptic Dysfunction, and Alzheimer's Disease.

Eric Tönnies1, Eugenia Trushina1,2

  • 1Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Journal of Alzheimer'S Disease : JAD
|January 7, 2017
PubMed
Summary

Oxidative stress contributes to synaptic dysfunction in Alzheimer's disease (AD) by increasing reactive oxygen species (ROS). Understanding this complex role is key to developing new AD therapies.

Keywords:
Alzheimer’s diseaseamyloid-βantioxidantscaloric restrictionexercisemitochondriamitohormesisneurotransmissionoxidative stresssynaptic functiontau protein

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder with no cure, where aging is the primary risk factor.
  • Synaptic loss strongly correlates with cognitive decline in AD, preceding neuronal death.
  • Oxidative stress, driven by increased reactive oxygen species (ROS), is implicated in aging and neurodegeneration, including AD.

Purpose of the Study:

  • To review the role of oxidative stress in synaptic dysfunction in Alzheimer's disease.
  • To discuss novel therapeutic strategies targeting the complex molecular mechanisms of AD.
  • To explore the dual role of ROS in both health and disease.

Main Methods:

  • Literature review focusing on oxidative stress, synaptic function, and Alzheimer's disease.
  • Analysis of molecular targets affected by ROS, including DNA, proteins, and cellular homeostasis.
  • Examination of the interplay between oxidative stress, amyloid-beta, and tau pathology.

Main Results:

  • Increased ROS production impairs synaptic activity and neurotransmission, leading to cognitive deficits.
  • ROS targets include nuclear and mitochondrial DNA, lipids, proteins, and calcium homeostasis.
  • A vicious cycle exists where cellular metabolism, Aβ, and tau pathology exacerbate mitochondrial dysfunction and ROS.

Conclusions:

  • Oxidative stress is a significant contributor to synaptic dysfunction in Alzheimer's disease.
  • Targeting oxidative stress pathways offers potential therapeutic avenues, despite mixed clinical trial results.
  • A comprehensive understanding of ROS's dual role is crucial for effective AD treatment development.