Previous works imply that involving brainstem in neuropathological studies of Alzheimer’s disease (AD) is of clinically significant. This work constructs a comprehensive neural mass model for cholinergic neuropathogenesis that involves brainstem, thalamus and cortex, wherein how acetylcholine deficiency in AD affects neural oscillation of the model output is systematically explored from the perspective of neurocomputation. By decreasing synapse connectivity parameters in direct cholinergic pathway from brainstem to thalamus or in indirect glutamatergic synapse pathway from cortex to brainstem to mimic the pathological condition of reduced acetylcholine release in patients with AD, the property of neural oscillation in this model is numerically investigated by means of power spectrum in frequency domain and amplitude distribution in time domain. Simulated results demonstrate that decreasing synapse connectivity whether in the direct cholinergic pathway or in the indirect glutamatergic synapse pathway can alter the neural oscillation significantly in three aspects: it induces an obvious decrease of dominant frequency; it leads to a degraded rhythmic activity in the alpha frequency band as well as an enhanced rhythmic activity in the theta frequency band; it results in reduced oscillation amplitude of the model output. These results are agreement with the characteristic of electrophysiological EEG measurement recorded in AD, especially support the hypothesis that cholinergic deficiency is a promising pathophysiological origin of EEG slowing in AD. Our analysis indicates that targeting the cholinergic system may have potential prospects in early diagnosis and treatment of AD.

Decreased coherence in electroencephalogram (EEG) has been reported in Alzheimer’s disease (AD) experimentally, which could be considered as a typical electrophysiological characteristic in AD. This work aimed to investigate the effect of AD on coherence in the dorsal visual pathway by the technique of neurocomputation. Firstly, according to the hierarchical organization of the cerebral cortex and the information flows of the dorsal visual pathway, a more physiologically plausible neural mass model including cortical areas v1, v2, and v5 was established in the dorsal visual pathway. The three interconnected cortical areas were connected by ascending and descending projections. Next, the pathological condition of loss of long synaptic projections in AD was simulated by reducing the parameters of long synaptic projections in the model. Then, the loss of long synaptic projections on coherence among different visual cortex areas was explored by means of power spectral analysis and coherence function. The results demonstrate that the coherence between these interconnected cortical areas showed an obvious decline with the gradual decrease of long synaptic projections, i.e. decrease in descending projections from area v2 to v1 and v5 to v2 and ascending projection from area v2 to v5. Hopefully, the results of this study could provide theoretical guidance for understanding the dynamical mechanism of AD.

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Previous works imply that involving brainstem in neuropathological studies of Alzheimer's disease (AD) is of clinically significant. Abnormality of cholinergic system also underlies the neurodegeneration during AD. This work constructs a comprehensive neural mass model for cholinergic neuropathogenesis that involves brainstem, thalamus and cortex, wherein how acetylcholine deficiency in AD affects neural oscillation of the model output is systematically explored from the perspective of neurocomputation. By decreasing synapse connectivity parameters in direct cholinergic pathway from brainstem to thalamus and indirect glutamatergic synapse pathway from cortex to brainstem to mimic the pathological condition of reduced acetylcholine release in patients with AD, the property of neural oscillation in this model is numerically investigated by means of power spectrum in frequency domain and amplitude distribution in time domain. Simulated results demonstrate that decreasing synapse connectivity whether in the direct cholinergic pathway or the indirect glutamatergic synapse pathway can alter the neural oscillation significantly in three aspects: it induces an obvious decrease of dominant frequency; it leads to a degraded rhythmic activity in alpha frequency band as well as an enhanced rhythmic activity in theta frequency band; it results in reduced oscillation amplitude of the model output. These results are agreement with the characteristic of electrophysiological EEG measurement recorded in AD, especially support the hypothesis that cholinergic deficiency is a promising pathophysiological origin of EEG slowing in AD. Our analysis indicates that targeting the cholinergic system may have potential prospects in early diagnosis and treatment of AD.