ArticleActa neuropathologica communications2018
Decoding the synaptic dysfunction of bioactive human AD brain soluble Aβ to inspire novel therapeutic avenues for Alzheimer's disease.
Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- Article
- Association of Aβ monomers with cerebral amyloid angiopathy in brains without parenchymal Aβ deposition.Brain communications · 2026Article
- Microglia across evolution: from conserved origins to functional divergence.Cellular & molecular immunology · 2025Review
- Modeling presynaptic inhibition by the amyloid precursor protein demonstrates one potential mechanism for preventing runaway synaptic modification in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Global C3 lowering in adulthood protects against hippocampal dysfunction and cognitive impairment in aged mice.Research square · 2025Article
- Varenicline Attenuates Memory Impairment in Amyloid-Beta-Induced Rat Model of Alzheimer's Disease.Neurochemical research · 2025Article
- Comparison of safety of lecanemab and aducanumab: a real-world disproportionality analysis using the FDA adverse event reporting system.Frontiers in pharmacology · 2025Article
- Real-Time Analysis of Neuronal Cell Cultures for CNS Drug Discovery.Brain sciences · 2024Article
- β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer's Disease.Nature communications · 2024Article
- Modeling the neuroimmune system in Alzheimer's and Parkinson's diseases.Journal of neuroinflammation · 2024Review
- A single-domain antibody detects and neutralises toxic AβAlzheimer's research & therapy · 2024Article
- Activation of βMolecular psychiatry · 2023Article
- Sugar distributions on gangliosides guide the formation and stability of amyloid-β oligomers.Biophysical chemistry · 2023Article
- Review
- Soluble and insoluble protein aggregates, endoplasmic reticulum stress, and vascular dysfunction in Alzheimer's disease and cardiovascular diseases.GeroScience · 2023Review
- Dietary glucosinolates derived isothiocyanates: chemical properties, metabolism and their potential in prevention of Alzheimer's disease.Frontiers in pharmacology · 2023Review
- Aβ oligomers from human brain impair mossy fiber LTP in CA3 of hippocampus, but activating cAMP-PKA and cGMP-PKG prevents this.Neurobiology of disease · 2022Article
- Bioactive human Alzheimer brain soluble Aβ: pathophysiology and therapeutic opportunities.Molecular psychiatry · 2022Review
- An ultra-sensitive immunoassay detects and quantifies soluble Aβ oligomers in human plasma.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Oxidative Stress and Beta Amyloid in Alzheimer's Disease. Which Comes First: The Chicken or the Egg?Antioxidants (Basel, Switzerland) · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Pathologic, biochemical and genetic evidence indicates that accumulation and aggregation of amyloid β-proteins (Aβ) is a critical factor in the pathogenesis of Alzheimer's disease (AD). Several therapeutic interventions attempting to lower Aβ have failed to ameliorate cognitive decline in patients with clinical AD significantly, but most such approaches target only one or two facets of Aβ production/clearance/toxicity and do not consider the heterogeneity of human Aβ species. As synaptic dysfunction may be among the earliest deficits in AD, we used hippocampal long-term potentiation (LTP) as a sensitive indicator of the early neurotoxic effects of Aβ species. Here we confirmed prior findings that soluble Aβ oligomers, much more than fibrillar amyloid plaque cores or Aβ monomers, disrupt synaptic function. Interestingly, not all (84%) human AD brain extracts are able to inhibit LTP and the degree of LTP impairment by AD brain extracts does not correlate with Aβ levels detected by standard ELISAs. Bioactive AD brain extracts also induce neurotoxicity in iPSC-derived human neurons. Shorter forms of Aβ (including Aβ
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