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Tau proteins, a class of microtubule-associated proteins (MAPs), are the central player in Alzheimer's disease and other neurodegenerative disorders. While most MAPs exist in all kinds of cells, Tau is present only in neurons and predominantly localized to the axon. The diseases caused by abnormal Tau proteins are collectively called tauopathy which is characterized by hyperphosphorylated Tau proteins. Phosphorylation refers to the addition of a phosphate group (PO43−) to an amino acid residue (particularly serine, threonine or tyrosine). In a hyperphosphorylated Tau protein, too many residues are phosphorylated so that the Tau protein can no longer bind the microtubule.
Tau Pathology Hotspots
In Alzheimer's disease, Tau abnormality typically begins in the entorhinal cortex, and then spreads to the hippocampus, thalamus, and cortical areas. Parkinson's disease is also associated with Tau pathology which occurs only in the striatum (Wills et al., 2010). This region plays a pivotal role in action selection: Go or NoGo, having direct connections with substantia nigra pars compacta whose impairment leads to the symptoms of Parkinson's disease. Tau pathology in the striatum has also been observed in frontotemporal dementia (Kim et al., 2007; Halabi et al., 2013). Furthermore, Huntington's disease is caused by the mutation of the protein, huntingtin, resulting in Tau pathology. Huntingtin is expressed ubiquitously across the brain, but the cerebral cortex, striatum, hippocampus and entorhinal cortex are the most severely affected (Vuono et al., 2015; L'Episcopo et al., 2016; Braak and Braak, 2015). The selective vulnerability coincides with the brain areas that may employ wireless communication (Section 10.2).
Locus coeruleus is an initiation area in the ascending arousal pathways. It exhibts hyperphosphorylated Tau in about 30% of cognitively unimpaired subjects, with ages ranging from 22 to 50 years upon death (Elobeid et al., 2012). This Tau pathology hotspot is implicated in all major neurodegenerative disorders, including Alzheimer's disease (Zarow et al., 2003), Parkinson's disease (Isaias et al., 2012), amyotrophic lateral sclerosis (Pamphlett and Kum Jew, 2013) and Huntington's disease (Zweig et al., 1992).
Regulation of Excitability by Tau
If Tau indeed plays a role in wireless communication, what is the underlying mechanism? In the brain, neuronal excitability is fundamentally governed by the opening and closing of ion channels, which in turn depends on membrane potential. The electromagnetic (EM) waves cannot modify directly the channel gating or membrane potential. Some kind of "transducer" is required to enable EM waves to modulate neuronal excitability. A possible mechanism has been proposed in the article, Microtubules As the Receiving Antennas. Figure 10-3 illustrates only the key concept.
The model was originally proposed to explain neuronal activation by EM force. Since the interaction among Ankyrin-G, EB1/3, and the microtubule fascicle can also be interfered by mechanical force such as ultrasound pressure, the same mechanism may apply to ultrasound stimulation. Focused ultrasound has been able to excite neurons in the cortical and subcortical brain structures (Kamimura et al., 2016). Remarkably, by focusing on the thalamus, a man could recover consciousness from coma (UCLA News).