Disrupted cross-laminar cortical processing in β amyloid pathology precedes cell death
Open accessAbstract
Disruption of neuronal networks in the Alzheimer-afflicted brain is increasingly recognized as a key correlate of cognitive and memory decline in Alzheimer patients. We hypothesized that functional synaptic disconnections within cortical columnar microcircuits by pathological β-amyloid accumulation, rather than cell death, initially causes the cognitive impairments. During development of cortical β-amyloidosis with still few plaques in the transgenic 5xFAD mouse model single cell resolution mapping of neuronal thallium uptake revealed that electrical activity of pyramidal cells breaks down throughout infragranular cortical layer V long before cell death occurs. Treatment of 5xFAD mice with the glutaminyl cyclase inhibitor, PQ 529, partially prevented the decline of pyramidal cell activity, indicating pyroglutamate-modified forms, potentially mixed oligomers of Aβ are contributing to neuronal impairment. Laminar investigation of cortical circuit dysfunction with current source density analysis identified an early loss of excitatory synaptic input in infragranular layers, linked to pathological recurrent activations in supragranular layers. This specific disruption of normal cross-laminar cortical processing coincided with a decline of contextual fear learning.
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Transgenic models show disruption of pyramidal cell activity prior to cell death with significant degeneration of synapses.
“Transgenic models show disruption of pyramidal cell activity prior to cell death 52 with significant degeneration of synapses. 53”
From Alzheimer's disease and its progression reduce pyramidal cell gain and connectivity (2025) · cites this paper as [52]
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- Authors
- Lison, H., Happel, M. F. K., Schneider, F., Baldauf, K., Kerbstat, S., Seelbinder, B., Schneeberg, J., Zappe, M., Goldschmidt, J., Budinger, E., Schröder, U. H., Ohl, F. W., Schilling, S., Demuth, H.-U., Scheich, H., Reymann, K. G., & Rönicke, R.
- Affiliations
- Leibniz Institute for Neurobiology (DE)
- German Center for Neurodegenerative Diseases (DE)
- Probiodrug (Germany) (DE)
- Corresponding author
- Rönicke, R.
- ORCID
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2014-03
- Volume
- 63
- Pages
- 62-73
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2035415625
- Cited by
- 23
- References
- 60
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 4
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Publikationsdatenbank der Fraunhofer-Gesellschaft (Fraunhofer-Gesellschaft) (submittedVersion)
- DZNE Pub (submittedVersion)
- Fraunhofer-Publica (Fraunhofer-Gesellschaft) (submittedVersion)
- Funders
- Alzheimer Forschung Initiative e. V. (10852)
- German Federal Ministry of Education and Science (VIP0562 — 03V0765)
- 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
- Alzheimer's disease, amyloid-beta, thallium uptake, 5xFAD mice, excitatory synaptic input, cognitive impairment, current source density
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Cerebral Cortex, Conditioning, Psychological, Disease Models, Animal, Fear, Fourier Analysis, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Neurons, Thallium, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Cell Death, Mice, Presenilin-1, Plaque, Amyloid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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