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Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

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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...
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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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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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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'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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Related Experiment Video

Updated: Apr 21, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
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Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease.

Shichun Tu1, Shu-ichi Okamoto, Stuart A Lipton

  • 1Neuroscience and Aging Research Center, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. shichuntu@sanfordburnham.org.

Molecular Neurodegeneration
|November 15, 2014
PubMed
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Alzheimer's disease involves amyloid-beta (Aβ) oligomers causing synaptic loss by overstimulating N-methyl-D-aspartate receptors (NMDARs). This leads to cognitive decline, but NMDAR antagonists show therapeutic promise.

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Area of Science:

  • Neuroscience
  • Pathology
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is characterized by synaptic and neuronal loss.
  • Soluble amyloid-beta (Aβ) oligomers are implicated in inducing synaptic loss in AD.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying Aβ-induced synaptic dysfunction.
  • To explore the role of N-methyl-D-aspartate receptors (NMDARs) in AD pathogenesis.
  • To identify potential therapeutic targets for mitigating Aβ-induced synaptic toxicity.

Main Methods:

  • Investigated the impact of Aβ oligomers on synaptic function and neuronal pathways.
  • Examined the role of NMDAR overstimulation and downstream signaling cascades.
  • Assessed the effects of NMDAR antagonists on Aβ-induced synaptic toxicity.

Main Results:

  • Aβ oligomers induce synaptic dysfunction via NMDAR overstimulation, leading to aberrant signaling pathways.
  • These pathways involve elevated cytoplasmic Ca2+, p-tau, caspases, and mitochondrial dysfunction.
  • Aβ also disrupts the scaffolding protein PSD-95, contributing to synaptic pathology.
  • NMDAR antagonists partially ameliorate Aβ-induced synaptic toxicity.

Conclusions:

  • Aβ-induced synaptic dysfunction is a complex process involving multiple interconnected pathways.
  • Aberrant NMDAR activation and PSD-95 dysregulation are key pathological events in AD.
  • Targeting NMDARs represents a potential therapeutic strategy for Alzheimer's disease.