ArticleFrontiers in computational neuroscience2014
Compensating for thalamocortical synaptic loss in Alzheimer's disease.
Article in Frontiers in 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.
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Who cites it
14 citing papers in PubMed.
- Investigating Gamma Frequency Band PSD in Alzheimer's Disease Using qEEG from Eyes-Open and Eyes-Closed Resting States.Journal of clinical medicine · 2025Article
- High-power transient 12-30 Hz beta event features as early biomarkers of Alzheimer's disease conversion: An MEG study.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- The possible connection between neutrophil-to-high-density lipoprotein ratio and cerebral perfusion in clinically established corticobasal syndrome: a pilot study.Frontiers in neurology · 2024Article
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- FNS allows efficient event-driven spiking neural network simulations based on a neuron model supporting spike latency.Scientific reports · 2021Article
- Decreased Alpha Peak Frequency Is Linked to Episodic Memory Impairment in Pathological Aging.Frontiers in aging neuroscience · 2021Article
- Opportunities for multiscale computational modelling of serotonergic drug effects in Alzheimer's disease.Neuropharmacology · 2020Review
- Competing Endogenous RNA Regulations in Neurodegenerative Disorders: Current Challenges and Emerging Insights.Frontiers in molecular neuroscience · 2018Review
- Disrupted Thalamus White Matter Anatomy and Posterior Default Mode Network Effective Connectivity in Amnestic Mild Cognitive Impairment.Frontiers in aging neuroscience · 2017Article
- Synaptic Impairment and Robustness of Excitatory Neuronal Networks with Different Topologies.Frontiers in neural circuits · 2017Article
- Article
- Atrophy of amygdala and abnormal memory-related alpha oscillations over posterior cingulate predict conversion to Alzheimer's disease.Scientific reports · 2016Article
- Sensorimotor cortex excitability and connectivity in Alzheimer's disease: A TMS-EEG Co-registration study.Human brain mapping · 2016Article
- Rhythmic Oscillations of Excitatory Bursting Hodkin-Huxley Neuronal Network with Synaptic Learning.Computational intelligence and neuroscience · 2016Article
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Authors and funding
3 authors.
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Abstract
The study presents a thalamocortical network model which oscillates within the alpha frequency band (8-13 Hz) as recorded in the wakeful relaxed state with closed eyes to study the neural causes of abnormal oscillatory activity in Alzheimer's disease (AD). Incorporated within the model are various types of cortical excitatory and inhibitory neurons, recurrently connected to thalamic and reticular thalamic regions with the ratios and distances derived from the mammalian thalamocortical system. The model is utilized to study the impacts of four types of connectivity loss on the model's spectral dynamics. The study focuses on investigating degeneration of corticocortical, thalamocortical, corticothalamic, and corticoreticular couplings, with an emphasis on the influence of each modeled case on the spectral output of the model. Synaptic compensation has been included in each model to examine the interplay between synaptic deletion and compensation mechanisms, and the oscillatory activity of the network. The results of power spectra and event related desynchronization/synchronization (ERD/S) analyses show that the dynamics of the thalamic and cortical oscillations are significantly influenced by corticocortical synaptic loss. Interestingly, the patterns of changes in thalamic spectral activity are correlated with those in the cortical model. Similarly, the thalamic oscillatory activity is diminished after partial corticothalamic denervation. The results suggest that thalamic atrophy is a secondary pathology to cortical shrinkage in Alzheimer's disease. In addition, this study finds that the inhibition from neurons in the thalamic reticular nucleus (RTN) to thalamic relay (TCR) neurons plays a key role in regulating thalamic oscillations; disinhibition disrupts thalamic oscillatory activity even though TCR neurons are more depolarized after being released from RTN inhibition. This study provides information that can be explored experimentally to further our understanding on the neurodegeneration associated with AD pathology.
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