ArticleJournal of computational neuroscience2014
Compensating for synaptic loss in Alzheimer's disease.
Article in Journal of computational neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- The Importance of Subjective Cognitive Decline Recognition and the Potential of Molecular and Neurophysiological Biomarkers-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Functional and Structural Changes in the Inner Ear and Cochlear Hair Cell Loss Induced by Hypergravity.International journal of molecular sciences · 2025Article
- Probing latent brain dynamics in Alzheimer's disease via recurrent neural network.Cognitive neurodynamics · 2024Article
- Article
- Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression.Frontiers in synaptic neuroscience · 2023Review
- Shaping a data-driven era in dementia care pathway through computational neurology approaches.BMC medicine · 2020Review
- Targeting the Synapse in Alzheimer's Disease.Frontiers in neuroscience · 2019Review
- Altered Neuronal Activity Topography Markers in the Elderly with Increased Atherosclerosis.Frontiers in aging neuroscience · 2017Article
- Changes of EEG Spectra and Functional Connectivity during an Object-Location Memory Task in Alzheimer's Disease.Frontiers in behavioral neuroscience · 2017Article
- Early Cerebellar Network Shifting in Spinocerebellar Ataxia Type 6.Cerebral cortex (New York, N.Y. : 1991) · 2016Article
- Abnormal Resting-State Functional Connectivity Strength in Mild Cognitive Impairment and Its Conversion to Alzheimer's Disease.Neural plasticity · 2016Article
- Theta and alpha EEG frequency interplay in subjects with mild cognitive impairment: evidence from EEG, MRI, and SPECT brain modifications.Frontiers in aging neuroscience · 2015Article
- Characterization of hippocampal Cajal-Retzius cells during development in a mouse model of Alzheimer's disease (Tg2576).Neural regeneration research · 2014Article
- Compensating for thalamocortical synaptic loss in Alzheimer's disease.Frontiers in computational neuroscience · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Confirming that synaptic loss is directly related to cognitive deficit in Alzheimer's disease (AD) has been the focus of many studies. Compensation mechanisms counteract synaptic loss and prevent the catastrophic amnesia induced by synaptic loss via maintaining the activity levels of neural circuits. Here we investigate the interplay between various synaptic degeneration and compensation mechanisms, and abnormal cortical oscillations based on a large-scale network model consisting of 100,000 neurons exhibiting several cortical firing patterns, 8.5 million synapses, short-term plasticity, axonal delays and receptor kinetics. The structure of the model is inspired by the anatomy of the cerebral cortex. The results of the modelling study suggest that cortical oscillations respond differently to compensation mechanisms. Local compensation preserves the baseline activity of theta (5-7 Hz) and alpha (8-12 Hz) oscillations whereas delta (1-4 Hz) and beta (13-30 Hz) oscillations are maintained via global compensation. Applying compensation mechanisms independently shows greater effects than combining both compensation mechanisms in one model and applying them in parallel. Consequently, it can be speculated that enhancing local compensation might recover the neural processes and cognitive functions that are associated with theta and alpha oscillations whereas inducing global compensation might contribute to the repair of neural (cognitive) processes which are associated with delta and beta band activity. Compensation mechanisms may vary across cortical regions and the activation of inappropriate compensation mechanism in a particular region may fail to recover network dynamics and/or induce secondary pathological changes in the network.
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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.