ArticleAnnals of neurology2011
Endogenous amyloid-β is necessary for hippocampal synaptic plasticity and memory.
Article in Annals of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
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Who cites it
151 citing papers in PubMed, 299 citations in OpenAlex.
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- α/Sulfonyl-γ-AApeptide foldamers mitigate Alzheimer's disease pathology by stabilizing transient helical domains in Aβ.Nature communications · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- The aging choroid plexus and its relationship with gut dysbiosis and Klotho decline: possible intervention strategies.GeroScience · 2025Review
- Neuroprotective Effects of Catechins by Differentially Affecting the Binding of Beta-amyloid and Its Aggregates to the Target Cells.Molecular neurobiology · 2025Article
- Physics of Protein Aggregation in Normal and Accelerated Brain Aging.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Alzheimer disease: Amyloid peptide controversies and challenges of anti-Aβ immunotherapy.The Journal of pharmacology and experimental therapeutics · 2025Review
- Neuronal and Glial α7 Nicotinic Acetylcholine Receptors: Role in Alzheimer's Disease Pathophysiology.Life (Basel, Switzerland) · 2025Review
- Neurotrophic and Neurotoxic Effects of Aβ42 and Its Oligomers on Neuronal Survival: Revealed by Their Opposite Influence on the Potency of Extracellular BDNF.International journal of molecular sciences · 2025Article
- Identification of isoAsp7-Aβ as a major Aβ variant in Alzheimer's disease, dementia with Lewy bodies and vascular dementia.Acta neuropathologica · 2024Article
- A Triple Mystery of Insidious Organ Failure: Are the Lung, Kidney and Brain All Damaged by the Ageing Pulse?Biomedicines · 2024Review
- The duality of amyloid-β: its role in normal and Alzheimer's disease states.Molecular brain · 2024Review
- Intracerebral inoculation of healthy non-transgenic rats with a single aliquot of oligomeric amyloid-β (1-42) profoundly and progressively alters brain function throughout life.Frontiers in aging neuroscience · 2024Article
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach.International journal of molecular sciences · 2023Review
- Alzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?Journal of advanced research · 2023Review
- Anti-Amyloid Therapies for Alzheimer's Disease and the Amyloid Cascade Hypothesis.International journal of molecular sciences · 2023Review
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
91 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveThe goal of this study was to investigate the role of endogenous amyloid-β peptide (Aβ) in healthy brain.
methodsLong-term potentiation (LTP), a type of synaptic plasticity that is thought to be associated with learning and memory, was examined through extracellular field recordings from the CA1 region of hippocampal slices, whereas behavioral techniques were used to assess contextual fear memory and reference memory. Amyloid precursor protein (APP) expression was reduced through small interfering RNA (siRNA) technique.
resultsWe found that both antirodent Aβ antibody and siRNA against murine APP reduced LTP as well as contextual fear memory and reference memory. These effects were rescued by the addition of human Aβ₄₂, suggesting that endogenously produced Aβ is needed for normal LTP and memory. Furthermore, the effect of endogenous Aβ on plasticity and memory was likely due to regulation of transmitter release, activation of α7-containing nicotinic acetylcholine receptors, and Aβ₄₂ production.
interpretationEndogenous Aβ₄₂ is a critical player in synaptic plasticity and memory within the normal central nervous system. This needs to be taken into consideration when designing therapies aiming at reducing Aβ levels to treat Alzheimer disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.