Acetylcholine Repairs the Amyloid-beta Damage on Brain Circuitry and Memory Loss From a “Mutated Biomimetic Acetylcholinesterase” Neuronal Memcapacitor During Slow-Wave Sleeping

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Amyloid-beta (A) plaque accumulation in the brain has been recognized to be associated with Alzheimer’s. Using artificial neuronal devices under controlled conditions, step-by-steps mimicking the A damages to neuronal circuitry is desirable, because of convenience without burdensome slicing and free from protein interference. We have developed nanostructured memcapacitor memory devices with a mutated biomimetic acetylcholinesterase (ACHE) neuron gorge; it serves as a model for testing memory dysfunction by a chronopotentiometry method and a cyclic voltammetry (CV) method with “sensory biomarks”. It is well known that ACH plays an important role in memory. Our “sensory-energy interaction map” was used to compare the results with and without ACH in NIST reference human serum. The results showed neuronal dysfunction in circadian rhythm (CRR) and memory reentrant before ACH was added and functional recovery after addition of 15 nM ACH. Mischief sensory-energy in three categories is restored. Our results showed ACH given at an early stage at Slow-Wave Sleeping (SWS) had greater chance to fully recover than at a late stage by rewiring the circuitry via formation of High Frequency Oscillation (HFO) that overcomes the Pathological High Frequency Oscillation (pHFO). Four stages of memory dysfunction caused by A are presented.

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Journal: TechConnect Briefs
Volume: 4, Advanced Manufacturing, Electronics and Microsystems: TechConnect Briefs 2015
Published: June 14, 2015
Pages: 226 - 229
Industry sectors: Advanced Materials & Manufacturing | Sensors, MEMS, Electronics
Topic: Nanoelectronics
ISBN: 978-1-4987-4730-1