ArticleeNeuro
3D Analysis of the Synaptic Organization in the Entorhinal Cortex in Alzheimer's Disease.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Neuroanatomical and psychological considerations in temporal lobe epilepsy.Frontiers in neuroanatomy · 2022Pooled it
- Distinct regional patterns of synaptic vulnerability across hippocampal and parahippocampal subregions in Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- Review
- Air pollution and Alzheimer disease phenotype deplete esterified proresolving lipid mediator reserves in the brain.JCI insight · 2025Article
- Volume electron microscopy reveals 3D synaptic nanoarchitecture in postmortem human prefrontal cortex.iScience · 2025Article
- Neurophysiological Progression in Alzheimer's Disease: Insights From Dynamic Causal Modelling of Longitudinal Magnetoencephalography.Human brain mapping · 2025Article
- Synapse vulnerability and resilience underlying Alzheimer's disease.EBioMedicine · 2025Review
- Volume electron microscopy reveals unique laminar synaptic characteristics in the human entorhinal cortex.eLife · 2025Article
- Early hippocampal hyperexcitability and synaptic reorganization in mouse models of amyloidosis.iScience · 2024Article
- Volume electron microscopy analysis of synapses in primary regions of the human cerebral cortex.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Key morphological features of human pyramidal neurons.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Unambiguous identification of asymmetric and symmetric synapses using volume electron microscopy.Frontiers in neuroanatomy · 2024Article
- Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer's disease.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Tau Oligomer-Containing Synapse Elimination by Microglia and Astrocytes in Alzheimer Disease.JAMA neurology · 2023Article
- Synaptic Compensatory Plasticity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Physiological Mechanisms Inherent to Diabetes Involved in the Development of Dementia: Alzheimer's Disease.Neurology international · 2023Review
- 3D synaptic organization of layer III of the human anterior cingulate and temporopolar cortex.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Spinal cord from body donors is suitable for multicolor immunofluorescence.Histochemistry and cell biology · 2023Article
- Spatial memory deficits in Alzheimer's disease and their connection to cognitive maps' formation by place cells and grid cells.Frontiers in behavioral neuroscience · 2022Review
- Emerging insights into synapse dysregulation in Alzheimer's disease.Brain communications · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The entorhinal cortex (EC) is especially vulnerable in the early stages of Alzheimer's disease (AD). In particular, cognitive deficits have been linked to alterations in the upper layers of EC. In the present report, we examined Layers II and III from eight human brain autopsies (four subjects with no recorded neurologic alterations and four AD cases). We used stereological methods to assess cortical atrophy of the EC and possible changes in the volume occupied by different cortical elements (neuronal and glial cell bodies; blood vessels; and neuropil). We performed 3D ultrastructural analyses of synapses using focused ion beam/scanning electron microscopy (FIB/SEM) to examine possible alterations related to AD. At the light microscope level, we found a significantly lower volume fraction occupied by neuronal bodies in Layer III and a higher volume fraction occupied by glial cell bodies in Layer II in AD cases. At the ultrastructural level, we observed that (1) there was a significantly lower synaptic density in both layers in AD cases; (2) synapses were larger and more complex in Layer II in AD cases; and (3) there was a greater proportion of small and simple synapses in Layer III in AD cases than in control individuals. These structural differences may play a role in the anatomic basis for the impairment of cognitive functions in AD.
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Registered trials
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