The Alzheimer’s Argument Against Immaterial Consciousness

Image credits belong to: aitoff | Pixabay

Prestigious philosophers have struggled to make sense of the mind as made up of matter/particles. Some have concluded that the mind must be immaterial or non-physical. In his defense of Christianity, James Porter Moreland states, “The soul has historically been understood as an immaterial substance that contains consciousness and animates the body or makes the body enlivened.” See the hyperlinked video here [1]. He denies that the “language of physical science” is useful for describing conscious states [2].

Our brain is the only organ housing and orchestrating our life of thoughts. I have no reason to believe there is a second house or orchestrator.

If consciousness is non-physical and immaterial, why do all of the various diseases that affect the brain and nervous system involve observable and molecular components? The anti-materialistic perspective has no anatomy or biology to show for the soul. It is vacuous for us to say humans possess a part for which we can locate no anatomy and biology. We are better off discussing the biology and anatomy that are observable.

Image credits belong to: geralt | Pixabay

In arguing that our mental states and consciousness are the outcome of material interactions, I would like to discuss some observable proteins. I also would like to discuss a particular brain disease. Suppose the brain has an immaterial basis, and there is an omnibenevolent deity responsible for that immaterial outcome. In that case, I find it hard to believe that Alzheimer's disease should be a necessary outcome.

Yes. I know. Here we are with the problem of evil again.

Spiral-shaped prion proteins are involved with the wretched Alzheimer's disease afflicting more than 5 million Americans [3]. Neurodegeneration is a prominent feature, which is simply the deprivation of nerve cell function and structure. The PrPc is a particle of normal character on the surface of your neurons, but it can mutate and misfold into the PrPsc (a scrapie form affecting sheep) that damages nearby cells [4]. The PrPc particles with normal, spiral-shaped, helical structures will make a different conformation with flattened beta strands that contribute to the disease. Analogously, PrPc particles are like opened metal chairs that cannot stack on top of each other [5]. If you tried, they would fall apart, unlike folded chairs that are stackable. You can aggregate them much like how these proteins will aggregate to form plaques.

These plaques that can appear like ugly brown spots in some images gather between neurons and obstruct cell function. These plaques deposit themselves after the breakdown of the amyloid precursor protein that is responsible for neurogenesis [6].

The protein-recycling machinery is disturbed by neurofibrillary tangles (unbreakable fibers forced out of their natural shape) formed by the aberrant folding of tau proteins [7]. Tau proteins hold together the microtubules like a railroad, allowing for cargo and nutrients between cells. In Alzheimer's, the tau proteins detach from the highway structure and cause the microtubules to fall apart into a catastrophe [8]. The tau strands float away to form the tangles. With no nutrient-carrying highway microtubules, there are no nutrients for the neuron. It therefore shrinks and disconnects from other neurons, leading to neuronal death and memory deprivation.

Image credits belong to: TheDigitalArtist | Pixabay

Many reports have focused on the hyperphosphorylation of tau proteins as a prominent feature of Alzheimer's disease. In the context of Alzheimer's disease, hyperphosphorylation is like having too much of a good thing [9]. Cellular processes must be phosphorylated in biology, meaning they must have phosphorus-oxygen groups attached to their molecules in relevance to regulating the mitotic part of the cell cycle. But when we add too many phosphorous-oxygen groups, we get the neurofibrillary tangles [10].

Contrary to this conventional understanding, findings from the Brain Mind Institute in Switzerland have shown that phosphorylation is not guaranteed to lead to those nasty fibrilized tangles despite causing tau proteins to unravel [11]. Reportedly, an inadequate resolution was involved with the many studies on hyperphosphorylation as a basis for tau pathology. The Brain Mind Institute scientists' new strategy used the K18 fragment of the tau protein responsible for fastening tau to microtubules. Their construction of K18 allowed them to have multiple vantage points to view the phosphorylation effects and observe tau clusters prevented by phosphorylation.

It is unclear to me how that unconventional understanding could change studies on Alzheimer's disease. Perhaps it will change everything we know about Alzheimer's. In the meantime, allow me to continue explaining several more things we have known until this point.

Inflammation is a key term I have heard concerning Alzheimer's disease throughout the years. Alzheimer's is driven by immune responses (which seems counterintuitive) that must employ pro-inflammatory agents to purge debris from the house, but this task later turns awry. Microglial cells and interleukin-1-beta are the pro-inflammatory heroes of immunity that become culprits in the mission later [12]. They arouse the kinases (chemical-reacting proteins that transfer phosphate groups) in tau proteins' pathological phosphorylation.

In 2013, scientists were interested in identifying these kinases. It was stated that these kinases could be "novel targets" for Alzheimer's disease [13]. The glycogen synthase kinase 3 beta (GSK3B) was said to be specifically responsible for phosphorylated tau in 2010 [14].

Hyperphosphorylated microtubules fall apart, causing the failure of nutrient-trafficking in the cell, which leads to the formation of oligomers (molecules with similar repeating units built from smaller molecules) that make the ugly, brown spotted plaques I mentioned earlier [15]. These oligomerized plaques and tau tangles place themselves in the cell's intracellular part to provoke cell death. The tangles can be ejected from the cell to act on and damage the microglial phagocytosis defense system that is meant to get rid of cellular debris and potentially trim away inefficient synapses in your early life [16]. The microglial phagocytosis defense system, which is meant to repair damaged sites, incites a kind of inflammation that does the opposite of its repair work.

Despite the many things we still have yet to understand about Alzheimer's, we at least know that these repeated episodes of neuronal death eventually shrink the cerebral cortex responsible for language and information-processing. The hippocampus that is in charge of making new memories will atrophy or waste away [17]. The gyri or ridges on the cerebral cortex will become smaller, and the sulci or grooves on the brain's surface will become larger.

We have amyloid precursor proteins (APP) located in our cell membranes. These APPs are meant to be healthy. Routinely, APPs must be scissored away by two different enzymes (beta-secretase and gamma-secretase) from the membrane. After cutting away from the two membrane sides, a peptide fragment of 38 amino acids can be easily metabolized and disposed of in a healthy brain [18]. However, in the Alzheimer's brain, there is a mutated gamma-secretase that cuts away a peptide of 42 amino acids (for mysterious reasons) and deposits the insoluble amyloid plaques [19]. Disruption in neurotransmitter communication is sure to follow.

This is relevant to the cholinergic hypothesis from the mid-1970's that focused on a specific enzyme called choline acetyltransferase (CHAT) that collects multiple entities together to make a neurotransmitter called acetylcholine (ACH) which is very crucial to your peripheral and central nervous system [20].

Within the cholinergic neurons of the cerebral cortex and hippocampus, the CHAT enzyme is dispatched from one end of a cholinergic neuron to the other end where the vesicle keeps the acetylcholine neurotransmitter [17]. Cholinergic neurons must use this acetylcholine to innervate nearly every brain region, especially for enabling you to pay attention, to learn new things, to remember things, to have stress responses, to remain awake, to fall asleep, and to sense information.

Deterioration of these cholinergic neurons plays a part in the memory deprivation of people living with Alzheimer's [17]. There is a disruption in the absorption of essential choline nutrients and a disruption to the nicotinic receptors that respond to acetylcholine for motor nerve-muscle communication.

If consciousness is immaterial/non-physical, it is strange that a disease such as Alzheimer's would manifest such visible and material effects/symptoms (e.g., anxiety, aggression, and mood and personality changes). Suppose consciousness is connected to some omnibenevolent deity. In that case, it is strange that he/she would allow a disease to steal from you the core and prominent features that make you human (e.g. memory loss, poor judgment, and inability to handle money) [22].

General Disclaimer: All sources are hyperlinked in this article. The author has made their best attempt to accurately interpret the sources used and preserve the source-author’s original argument while avoiding plagiarism. Should you discover any errors to that end, please email thecommoncaveat@gmail.com and we will review your request.

All information in this article is intended for educational/entertainment purposes only. This information should not be used as medical/therapeutic advice. Please seek a doctor/therapist for health advice.

Works cited:

[1] Neuroscience and the Soul - Full Interview with J.P. Moreland - YouTube

[2] Arguing God from Consciousness? - J.P. Moreland | Closer to Truth

[3] Alzheimer's Facts and Figures Report | Alzheimer's Association

[4] Prions-What are they ? Protein Misfolding Mechanism - YouTube

[5] Prions | The General Mechanism of Prion Formation and Disease - YouTube

[6] What Happens to the Brain in Alzheimer's Disease? | National Institute on Aging (nih.gov)

[7] Amyloid Plaques and Neurofibrillary Tangles | BrightFocus Foundation

[8] Inside the Brain: Unraveling the Mystery of Alzheimer's Disease [HQ] - YouTube

[9] Hyperphosphorylation - Wikipedia

[10] Neurofibrillary tangle - Wikipedia

[11] A new perspective on the role of phosphorylation in Alzheimer’s and other tau pathologies | Research Square