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Related Concept Videos

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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.
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Related Experiment Video

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Infliximab ameliorates AD-associated object recognition memory impairment.

Dong Hyun Kim1, Seong-Min Choi2, Jihoon Jho3

  • 1Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University, Busan, 49315, Republic of Korea.

Behavioural Brain Research
|June 7, 2016
PubMed
Summary

Alzheimer's disease impairs visual memory via amyloid-beta (Aβ) oligomers affecting synaptic plasticity in the perirhinal cortex. Infliximab treatment reversed these deficits by targeting TNF-α-mediated inflammation.

Keywords:
Alzheimer’s diseaseInfliximabMuscarinic acetylcholine receptor-dependent long-term depressionVisual recognition memory

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Area of Science:

  • Neuroscience
  • Pathology
  • Immunology

Background:

  • Perirhinal cortex (PRh) dysfunction is linked to visual recognition memory deficits in early Alzheimer's disease (AD).
  • Muscarinic acetylcholine receptor-dependent long-term depression (mAChR-LTD) is crucial for memory formation.
  • Tg2576 mice show impaired mAChR-LTD due to amyloid-beta (Aβ) oligomers.

Purpose of the Study:

  • To investigate the impact of Aβ oligomers on visual recognition memory and PRh synaptic function.
  • To determine the role of TNF-α in Aβ-induced memory impairment and synaptic dysfunction.
  • To evaluate the therapeutic potential of infliximab in an Aβ-induced mouse model.

Main Methods:

  • Administration of Aβ oligomers to young normal mice.
  • Assessment of visual recognition memory.
  • Electrophysiological recordings of mAChR-LTD in mouse PRh slices.
  • Treatment with infliximab, an anti-TNF-α monoclonal antibody.

Main Results:

  • Aβ oligomers impaired visual recognition memory and perturbed mAChR-LTD in mouse PRh.
  • Infliximab treatment significantly improved memory deficits induced by Aβ oligomers.
  • Infliximab annulled the detrimental effects of Aβ on mAChR-LTD.

Conclusions:

  • Aβ-induced inflammation, mediated by TNF-α signaling, disrupts synaptic transmission in the PRh.
  • This disruption leads to visual recognition memory deficits characteristic of early Alzheimer's disease.
  • Targeting TNF-α represents a potential therapeutic strategy for Alzheimer's disease-related memory impairments.