Multi-site dynamic recording for Aß oligomers-induced Alzheimer's disease in vitro based on neuronal network chip.

Alzheimer's disease (AD) is a chronic central neurodegenerative disease. The pathological features of AD are the extracellular deposition of senile plaques formed by amyloid-ß oligomers (AßOs) and the intracellular accumulation of neurofibrillary tangles. However, due to the lack of effective method and experimental models to study the cognitive decline, communication at cell resolution and the implementation of interventions, the diagnosis and treatment on AD still progress slowly. In this paper, we established a pathological model of AD in vitro based on AßOs-induced hippocampal neuronal network chip for multi-site dynamic analysis of the neuronal electrical activity and network connection. The multiple characteristic parameters, including positive and negative spike intervals, firing rate and peak-to-peak values, were extracted through the analysis of spike signals, and two firing patterns from the interneurons and pyramidal neurons were recorded. The spatial firing patterns mapping and cross-correlation between channels were performed to validate the degeneration of neuronal network connectivity. Moreover, an electrical stimulation with frequency at 40 Hz was exerted to preliminarily explore the therapeutic effect on the pathological model of AD. This neuronal network chip enables the implementation of AD models in vitro for studying basic mechanisms of neurodegeneration within networks and for the parallel testing of various potential therapies. It can be a novel technique in the research of AD pathological model in vitro.

Chronic noise exposure and Alzheimer disease: Is there an etiological association?

Recent work has implicated environmental stimuli as contributing to the risk of developing Alzheimer's disease (AD). Noise is one of the most important environmental health hazards for humans. Here, we propose that noise exposure, especially chronic noise exposure, can cause AD-like neuropathological changes, and that persistence of these changes have an etiological association with the development of AD. Noise can induce tau hyperphosphorylation, formation of neurofibrillary tangles (NFT) and increase ß-amyloid (Aß) and amyloid precursor protein (APP) and thus could be pivotal to AD pathogenesis and progression. The aberrant accumulation of NFT and Aß could promote synaptic malfunction and apoptosis of neurons, which eventually could lead to Alzheimer dementia. Noise-induced excitotoxicity and oxidative stress are associated with AD-like neuropathology and an increasing risk for the development of AD. Noise can induce excitotoxicity and oxidative stress which might be one of the mechanisms how noise exposure could increase AD risk. To test this hypothesis, epidemiological studies should be carried out. On the other hand, in addition to its potential risk for the development of AD, noise exposure has many other harmful effects which warrant that actions should be taken to protect the public health from noise hazards without waiting for the results of these studies.

Induction of RhoGAP and pathological changes characteristic of Alzheimer's disease by UAHFEMF discharge in rat brain.

Novel experiments with Ultrasound Associated with High Frequency Electromagnetic Field (UAHFEMF) irradiation on rats and mice found evidences of characteristic Alzheimer's disease (AD) degenerations including neurite plaques, beta-amyloid, TAU plaque and deposition in cells, Neuro-Fibrillary Tangle and Paired Helical Filament (PHF) with rats and mice irradiated up to 2454 hours. Concomitant passive avoidance test was performed on six mice, and all showed signs of visual and auditory agnosia and lost cognition of threatening condition. The post section Thioflavin-S fluorescent microscopy found dilated ventricles and dense amyloid-deposition in Ca3 and dentate gyrus. In addition, PHF was identified in the 2454 hours-irradiated rat brain by electron microscope. A human T-cell activation RhoGTPase-activating protein (TAGAP) isoform b homolog (GenBank accession # P84107) induced in the UAHFEMF-treated rat brain was identified using electron spray ionization (ESI) liquid chromatography tandem mass spectrometry (LC/MS/MS). We hypothesized that one of the causes of AD can be the UAHFEMF discharges in human brain.