Microtubules the seat of Consciousness

[citizenschallengev4]

Right so let’s get it back on track.
Along with an apology, you are correct, I didn’t really notice, or read this paper where you first posted it, because frankly it’s irrelevant to that particular discussion.

Although you are correct, it still seems to me, this is about the systems and mechanics of the brain and the process of producing thoughts,
Bringing it back to the point about microtubules being an essential component (widget) of the process of thinking and consciousness -
but that to understand consciousness itself, especially higher levels of complex consciousness, that requires more than simply recognizing microtubules contribution within the outrageously complex system.

I’ve taken the liberty of moving the following post from the thread discussion, where it didn’t belong, over here, since this is really proper thread for this contribution to our debate.

@write4u

@citizenschallengev4

Do we really?
Where are your papers on that - and please not another paper on microtubules and mitosis! When you’re supposedly to be discussing better understanding of our consciousness.

Here again I’ll bet you are elevating assumptions, and the usual PR driven hopes, to the level of certitude, when it’s no more than dreams at this point.

Obviously you do NOT read everything I post or you would not be asking such a fundamental question which I have already answered several times.

But I’m glad to provide proof of that claim.

Enhancing microtubule stabilization rescues cognitive deficits and ameliorates pathological phenotype in an amyloidogenic Alzheimer’s disease model

• Juan Jose Fernandez-Valenzuela,
• Raquel Sanchez-Varo, * Clara Muñoz-Castro, * Vanessa De Castro, * Elisabeth Sanchez-Mejias, * Victoria Navarro, * Sebastian Jimenez, * Cristina Nuñez-Diaz,
• Angela Gomez-Arboledas, * Ines Moreno-Gonzalez, * Marisa Vizuete, * Jose Carlos Davila, * [Javier Vitorica] Enhancing microtubule stabilization rescues cognitive deficits and ameliorates pathological phenotype in an amyloidogenic Alzheimer’s disease model | Scientific Reports) & * Antonia Gutierrez

Abstract

In Alzheimer’s disease (AD), and other tauopathies, microtubule destabilization compromises axonal and synaptic integrity contributing to neurodegeneration. These diseases are characterized by the intracellular accumulation of hyperphosphorylated tau leading to neurofibrillary pathology. AD brains also accumulate amyloid-beta (Aβ) deposits. However, the effect of microtubule stabilizing agents on Aβ pathology has not been assessed so far. Here we have evaluated the impact of the brain-penetrant microtubule-stabilizing agent Epothilone D (EpoD) in an amyloidogenic model of AD. Three-month-old APP/PS1 mice, before the pathology onset, were weekly injected with EpoD for 3 months.

Treated mice showed significant decrease in the phospho-tau levels and, more interesting, in the intracellular and extracellular hippocampal Aβ accumulation, including the soluble oligomeric forms.

Moreover, a significant cognitive improvement and amelioration of the synaptic and neuritic pathology was found. Remarkably, EpoD exerted a neuroprotective effect on SOM-interneurons, a highly AD-vulnerable GABAergic subpopulation. Therefore, our results suggested that EpoD improved microtubule dynamics and axonal transport in an AD-like context, reducing tau and Aβ levels and promoting neuronal and cognitive protection.

These results underline the existence of a crosstalk between cytoskeleton pathology and the two major AD protein lesions. Therefore, microtubule stabilizers could be considered therapeutic agents to slow the progression of both tau and Aβ pathology.

more…
Enhancing microtubule stabilization rescues cognitive deficits and ameliorates pathological phenotype in an amyloidogenic Alzheimer’s disease model | Scientific Reports

Alzheimer disease (AD) is a member of a category of neurodegenerative disorders called tauopathies (Wang and Liu, 2008).

Figure 1

Microtubules in axons and dendrites consist of a stable region towards the minus end of the microtubule and a labile region towards the plus end, as well as a pool of free tubulin subunits. Microtubule severing is a normal event in the neuron, when tightly regulated. Abnormal (deregulated) microtubule severing is posited to account for microtubule loss in AD. Severing in the stable region of the microtubule would create two new microtubules, with fairly minimal disassembly of either one. Severing in the labile region of the microtubule would result in notably more disassembly. Severing at the end of the microtubule would result in disassembly. Because known microtubule-severing proteins favour the stable region of the microtubule, treatment of AD with a microtubule-stabilizing drug may mitigate disassembly that occurs as an aftereffect of the severing, but the severing events themselves would likely increase.*

more…

It cuts two ways: microtubule loss during Alzheimer disease - PMC

There are several pages in Google search alone that discuss the link between microtubule catastrophe and neural (mental) degeneration.

Alzheimer’s is just one out of a dozen or so mental degradation diseases caused by
microtubule failure.
There is no doubt that microtubules are intimately connected with brain functions and access to consciousness.

Accept that proven fact and the rest becomes a lot easier. This is not a belief, this is proven and applied science.

The Biology of General Anesthesia from Paramecium to Primate

Anesthetics bind to tubulin, causing microtubules to destabilize** [84,85]. They can also cause microtubule-based molecular motors, such as kinesin, to reversibly fall off the micro- tubule lattice and thus disrupt transport of vesicles, proteins, and organelles to synapses [86].Nov 18, 2019

https://www.cell.com/current-biology/pdf/S0960-9822(19)31262-X.pdf

Okay, I stand corrected in so far a this paper and its limited implications.