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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'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...
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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...
Long-term Depression01:03

Long-term Depression

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.
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression01:05

Long-term Depression

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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Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...

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Related Experiment Video

Updated: May 19, 2026

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies
10:08

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies

Published on: July 20, 2022

Targeting synaptic dysfunction in Alzheimer's disease therapy.

Robert Nisticò1, Marco Pignatelli, Sonia Piccinin

  • 1Department of Pharmacobiology, University of Calabria, 87036 Rende, Italy. r.nistico@med.uniroma2.it

Molecular Neurobiology
|August 24, 2012
PubMed
Summary
This summary is machine-generated.

Researchers explored Alzheimer's disease (AD) using mouse models to understand synaptic dysfunction and test therapies. Despite promising preclinical results, translating these findings into effective human treatments remains challenging.

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Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
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Last Updated: May 19, 2026

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies
10:08

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Published on: July 20, 2022

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Alzheimer's disease (AD) research focuses on genetics and molecular pathogenesis.
  • Transgenic (Tg) mouse models are crucial for studying AD progression and testing interventions.
  • Synaptic dysfunction and synapse loss are strongly linked to cognitive decline in AD.

Purpose of the Study:

  • To review synaptic alterations in various AD animal models.
  • To summarize pharmacological strategies targeting synaptic plasticity in AD.
  • To discuss limitations in translating preclinical findings to human clinical trials.

Main Methods:

  • Utilizing transgenic (Tg) mouse models and non-Tg models with amyloid-beta (Aβ) application.
  • Conducting electrophysiological studies to assess hippocampal synaptic transmission and long-term potentiation.
  • Evaluating the efficacy of pharmacological interventions in AD models.

Main Results:

  • Numerous pharmacological interventions have shown potential in attenuating synaptic dysfunction and improving behavior in AD models.
  • Preclinical studies demonstrate promise in rescuing hippocampal plasticity phenotypes.
  • Significant challenges exist in translating these experimental findings into human clinical applications.

Conclusions:

  • Synaptic dysfunction is a key feature in Alzheimer's disease animal models.
  • While numerous therapeutic strategies show promise in preclinical settings, successful translation to human treatments is limited.
  • Limitations in experimental systems pose significant hurdles for developing effective disease-modifying therapies for Alzheimer's disease.