Amyloid-β–induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks
Open accessAbstract
Alzheimer's disease is the most frequent neurodegenerative disorder and the most common cause of dementia in the elderly. Diverse lines of evidence suggest that amyloid-beta (Abeta) peptides have a causal role in its pathogenesis, but the underlying mechanisms remain uncertain. Here we discuss recent evidence that Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. Strategies that block these Abeta effects may prevent cognitive decline in Alzheimer's disease. Potential obstacles and next steps toward this goal are discussed.
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Aβ accumulation is associated with perturbations in synaptic function, neuronal loss, and memory and cognitive impairments.
“Aβ accumulation is associated with perturbations in synaptic function, neuronal loss, and memory and cognitive impairments (Lue et al., 1999; Akiyama et al., 2000b; Palop and Mucke, 2010).”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Palop and Mucke, 2010
The Introduction and “Modulation of synaptic transmission by Aβ” sections link elevated Aβ to impaired synaptic function and synaptic loss. “Elevated Aβ destabilizes neural network activity” links these changes to learning, memory, and cognitive deficits. The passages describe loss of synapses, not loss of neurons, so they do not support that part of the claim; page numbers were not provided in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLFP recording showed E3S/S mice are protected against tau-induced deficits in theta and gamma oscillations at 6-7 months of age before tau-induced neurodegeneration at 9 months of age.
“LFP recording of network activities showed that E3S/S mice are protected against tau-induced deficits in theta and gamma oscillations at 6–7 months of age before tau-induced neurodegeneration at 9-months of age, suggesting that network dysfunction represents early pathogenetic mechanisms in AD48.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [48]
The section ‘Elevated Aβ destabilizes neural network activity’ reports abnormal network activity in Alzheimer’s-related hAPP mice, supporting the sentence’s general point about network dysfunction. It does not report LFP recordings in E3S/S mice, protection from tau-induced theta or gamma deficits at 6–7 months, or neurodegeneration at 9 months (page unavailable in our copy). (LLM, conf=0.82)
Experimental — accuracy not yet measuredNetwork dysfunction represents early pathogenetic mechanisms in AD.
“LFP recording of network activities showed that E3S/S mice are protected against tau-induced deficits in theta and gamma oscillations at 6–7 months of age before tau-induced neurodegeneration at 9-months of age, suggesting that network dysfunction represents early pathogenetic mechanisms in AD48.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [48]
The Introduction and ‘Elevated Aβ destabilizes neural network activity’ section link abnormal network activity to Alzheimer’s-related pathology and possible cognitive decline. They support a pathogenetic role for network dysfunction, but do not establish that it is an early mechanism preceding neurodegeneration. The preceding tau-mouse findings are the citing authors’ own results, not a claim attributed to this source. (LLM, conf=0.82)
Experimental — accuracy not yet measuredNetwork dysfunction represents early pathogenetic mechanisms in AD.
“supporting the notion that network dysfunction represents early pathogenetic mechanisms in AD46”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [46]
The section 'Elevated Aβ destabilizes neural network activity' proposes that aberrant network activity contributes to cognitive decline, supporting a role for network dysfunction in AD pathogenesis. It does not establish that network dysfunction is an early mechanism in the disease course; the paper also identifies the relationship between network alterations and cognitive function as an unresolved issue. No page numbers were available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAD patients and AD mouse models display excitation/inhibition circuit imbalances that affect the oscillatory patterns underlying cognitive processing.
“AD patients and AD mouse models display excitation/inhibition circuit imbalances that affect the oscillatory patterns underlying cognitive processing 106, 107 .”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [107]
People with Alzheimer's disease have more seizures than non-demented controls.
“Similarly, individuals with Alzheimer’s disease experience increased incidence of seizures compared with non-demented controls, suggesting that Alzheimer’s disease pathology may be involved in destabilizing broad neuronal networks100.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [100]
Alzheimer's disease pathology may destabilize widespread neuronal networks.
“Similarly, individuals with Alzheimer’s disease experience increased incidence of seizures compared with non-demented controls, suggesting that Alzheimer’s disease pathology may be involved in destabilizing broad neuronal networks100.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [100]
10-22% of Alzheimer's disease patients exhibit seizures, as do hAPPFAD mice, and the onset of these seizures precedes cognitive decline.
“10–22% of AD patients exhibit seizures [98–100], as do hAPPFAD mice [101], and the onset of these seizures precedes cognitive decline [102].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [99]
Mouse models indicate alterations in synaptic networks prior to the onset of gross neuronal loss in the cerebral cortex.
“A growing body of evidence in mouse models indicates alterations in synaptic networks, prior to the onset of gross neuronal loss in the cerebral cortex [140, 141].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [140]
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Hierarchical Organization of Tau and Amyloid Deposits in the Cerebral Cortex
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Cerebral white matter lesions – associations with Aβ isoforms and amyloid PET
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An Unbalanced Synaptic Transmission: Cause or Consequence of the Amyloid Oligomers Neurotoxicity?
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Down-regulated expression of microRNA-338-5p contributes to neuropathology in Alzheimer’s disease.
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- Authors
- Palop, J. J., & Mucke, L.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Palop, Jorge J
- Mucke, Lennart
- Venue
- Nature Neuroscience
- Published
- 2010-06-25
- Volume
- 13
- Issue
- 7
- Pages
- 812-818
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3072750
- OpenAlex
- W2131180711
- Cited by
- 1,651
- References
- 77
- Citations by year
- 2026: 81 · 2025: 100 · 2024: 102 · 2023: 88 · 2022: 119 · 2021: 120 · 2020: 120 · 2019: 90 · 2018: 127 · 2017: 113 · 2016: 134 · 2015: 89 · 2014: 117 · 2013: 99 · 2012: 81
- FWCI
- 8.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG022074, P01AG022074)
- National Institute of Neurological Disorders and Stroke (R01NS041787, NS041787)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta, Alzheimer's disease, synaptic dysfunction, artificial neural networks, presynaptic modulation, postsynaptic regulation, excitatory synaptic transmission, amyloid-beta oligomers, epileptiform discharges, inhibitory interneurons, neuronal synchronization, cognitive decline
- MeSH terms
- Alzheimer Disease, Humans, Neural Pathways, Synaptic Transmission, Synapses, Amyloid beta-Peptides
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