Alzheimer’s Argument Against the Soul—Part 2
Read this first: The Alzheimer’s Argument Against Immaterial Consciousness — The Common Caveat
Introduction
In a previous post, I defended a physicalist/materialist view of consciousness. I used Alzheimer's Disease as an example of a physical event resulting in the loss of consciousness. I aimed my argument at Christian apologist J.P. Moreland's linking of consciousness with the soul as an immaterial substance. I want to advance my argument in this article by discussing the genetics of Alzheimer's Disease.
Allow me to state my premises clearly:
Syllogism 1:
Premise 1: Anything that takes up space and has mass is considered matter.
Premise 2: DNA and genes take up space and have mass.
Conclusion: DNA and genes are examples of matter.
Syllogism 2:
Premise 1: The brain and nervous system contain
DNA and genes as material components.
Premise 2: The brain and nervous system supply us with consciousness.
Conclusion: Consciousness is material.
The neurodegeneration of Alzheimer's Disease is a great example of insidious loss of consciousness, according to John K Grandy's abstract in a 2015 report titled Alzheimer Disease and Human Consciousness: A Neurogenetic Connection.
In my previous article, I stated about the beta-amyloid plaques (clumps formed from the gathering of sticky fragments cut from larger proteins) that injure the neurons and shrink brain volume. I used this as an example of material consciousness at work.
I gather from John K Grandy that there is a lack of unanimity across professional fields regarding how we should define consciousness. A philosopher, a psychologist, and a neurobiologist may each define consciousness differently. However, Grandy proposes the following:
"...A basic and comprehensive definition of human consciousness could be- a collective totality of awareness, bodily (or somatic) sensations, perceptions (sensory input and neurobiological information), emotions, thoughts, and recollections of the self within a moment on the time continuum."
He then states three fundamental notions about consciousness:
"1) consciousness emerges quite simply from an understanding of neuronal activity 2) consciousness is not a discrete operation of the brain, but rather, the outcome of computational activity of the associated areas of the brain 3) consciousness is a discrete phenomenon and that the issues of subjectivity, unity, and intentionality must be confronted if we are to understand how our experience is constructed."
I want to use Francis Crick and Christopher Koch's 1990s neural correlates of consciousness (NCC) as some groundwork. The NCC are the tiniest amount of neural parts cooperating together, just enough for you to engage with the world around you. Brains systems are operating alongside your conscious experience, which is "your individual awareness of your unique thoughts, memories, feelings, sensations, and environments." The NCC helps us discriminate the conscious neural workings from the unconscious neural workings.
The following are four examples of NCC as stated by Grandy:
Anesthesia is said to impact the frontal cortex (responsible for enabling you to do tricky things when they are very necessary) and the posterior parietal cortex (important for movement, attention, and perceiving 3-dimensional objects).
2. PET scans and functional MRI technology have been used on patients in a minimally conscious state (i.e., consciousness is intensely altered but there is still slight awareness of self and environment) and patients with unresponsive wakefulness syndrome (i.e., coming out of a coma with their eyes open but cannot respond to commands). The technology has revealed a reduction in communications between the cerebrum and other brain areas.
3. The frontoparietal network, which is said to be a core executor of uninterrupted attention and complex problem-solving, is also responsible for accessing information from non-conscious parts of the brain and then disseminating it to other regions (i.e., global workspace theory). The external sensory awareness suppliers (i.e., lateral prefrontal and parietal cortices) and the internal awareness suppliers (i.e., precuneal and mesiofrontal midline activity) are essential to your frontoparietal network.
4. The thalamocortical regions (tree-like fibers between the thalamus and cerebral cortex) are demonstrable suppliers of important "emergent properties of collective widespread connectivity of consciousness."
There are electric correlates of consciousness according to what is revealed by high-density electroencephalography (HD-EEG). Scientists can observe the brain's electric responses to stimuli. This technology allows us to view human consciousness based on interactions between the brain, spinal cord, peripheral nerves, and sensory organs.
DNA is Grandy's answer as to what lies beneath the network of brain regions and neuronal passages. There is a neurogenetic description of human consciousness. This includes genes and the biochemical stuff used to encode information in a gene to assemble protein molecules. What comes to mind are the transcription factors that switch genes "on" and "off." These impact the neurobiology of your consciousness.
The DNA that generates human consciousness and provides a continuous sequence of conscious events can also play a part in the neuronal failure that is so characteristic of Alzheimer's Disease.
According to Grandy, human consciousness has three neurogenetic phases:
Neurogenetic Phase 1
The inception of neuron-based consciousness is the first phase which happens at the inception of master genes that code for big-scale traits (head, tail, wings, arms, etc.) and "transactivate genes downstream." What happens next is a cascade of gene expression and multistep signaling pathways that include communications based on two purines (two-ringed, water-soluble, organic compounds) and two pyrimidines (colorless crystalline compounds).
Here are some first phase genes that generate brain regions of consciousness:
Pax6 is an important protein said to switch on the genes that sculpt the eyes, brain, spinal cord, and pancreas during embryonic development. Pax6 helps to develop the olfactory bulb of brain cells specialized for processing smell. Pax6 can advance the neurogenic fates of the neural progenitor cells that divide a limited number of times and transform into glial cells that hold nerve cells in place.
Otx1- Grandy states that this orchestrates 80% of cerebral cortex size. In 2003, Otx1 was reported to have an "unsuspected role" in pluripotent blood cell formation.
Otx2- this is a member of the homeobox family acting early in embryonic development to supply the optic nerves that carry information from the eyes to the brain. It helps to form your pituitary gland, which generates hormones that control growth and reproduction. The Otx2 helps develop the diencephalon, which is a division of the forebrain attaching the optic nerve responsible for vision and sight. The Otx2 helps develop the mesencephalon, one of the primary vesicles involved with the neural tube that precedes brain and spinal cord development. Later, it forms into the highest part of the brainstem. Otx2 helps develop the telencephalon, which includes convoluted gray matter on the brain's outermost layer, the hippocampus responsible for memory, and the basal ganglia important for voluntary movement.
Pax3- this is a master gene operating in neural crest cells traveling from the growing spinal cord to particular embryonic regions. The Pax3 gene will make a protein that guides other genes to signal neural crest cells to form the melanocytes that contribute to hair, eyes, and skin colors. Pax3 is also responsible for craniofacial bone formation and myogenesis (muscle tissue formation).
Pax3 affects the following genes downstream:
The tumor suppressor gene 53 is prominently involved with cell division and cell death.
The Hes1 protein is key to cell cycle arrest, self-renewal, getting rid of abnormal cells, and changing cells from one type to another.
The Neurog2 gene encodes for a protein momentous to neurogenesis.
The Meis2 gene regulates the copying of DNA segments into RNA.
Neurogenetic Phase 2:
The genome must operate correctly for there to be a continuum of neuron-based consciousness. Its communication system is made of nucleotides that are the monomeric units of the DNA and RNA molecules imperative for all Earthly lifeforms. Important to studying the second neurogenetic phase is the genetic basis of neuron plasticity (your brain's ability to regrow and reorganize neural networks) and abnormal conditions caused by gene and chromosome changes, as seen in specific psychiatric disorders (e.g., schizophrenia and autism).
These neuron plasticity genes are examples of genes in the second phase:
Brain-derived neurotrophic factor (BDNF) is a protein engaged at the synapses between nerve cells. It helps neurons attain maturation, growth, and maintenance. This protein manages the synaptic adaptability that is vital for learning and memory.
The fibroblast growth factor (FGF2) encodes for cell-to-cell communication, cell proliferation, replacement of damaged tissue, and cells' transformation into other types.
Delta-FosB is one of the many transcription factors involved with the brain's reward system during recurring contact with abused drugs. It brings about the sensitized responses to drugs. It is a very stable protein upon which drugs establish their enduring damage to your gene expression or process by which information from genes is used to synthesize products/proteins.
Synapsins- these are proteins involved with the transmission and formation of synapses. They govern neurotransmitter release, how synaptic efficacy changes over time, and the vesicles that transport materials between cells.
Deletion of a very crucial gene located on the X chromosome is associated with autism. It is the PTCHD1 gene that encodes a protein similar to those found in lab-model fruit flies (Drosophila). The encoded Drosophila proteins act as receptors (responders to light and transmitters of signals to sensory nerves) for the morphogens (determinants of tissue development patterns) of the sonic hedgehog signaling pathways that transmit genetic information from the mother to the embryo.
Three genes are correlated with schizophrenia:
1) Phosphodiesterase 4B- this involves an encoded protein that manages the bond arrangements between sugar and phosphate groups concentrated in your cells. The encoded protein is also involved with the chemical and physical signals sent through your cells in a series of molecular events.
2) Disrupted in schizophrenia 1 (DISC1)- this is a protein stated to take part in managing the cells' increase in number, the cells' transformations into other types, the cells' directed movements in response to chemical and mechanical signals, and the outgrowth of axons and dendrites, among other things. Alterations of the protein structure are stated to increase susceptibility to schizophrenia.
3) The ZNF804a is a nuclear protein suspected of causing susceptibility to schizophrenia, based on genome-wide association studies. ZNF804a is stated to interact with other proteins that neuronally remove introns from messenger RNA strings. ZNF804a also contacts proteins that attach to the double or single-stranded RNA, one of which is the RBFOX1 associated with schizophrenia.
Neurogenetic Phase 3:
If human consciousness was not rooted in observable materials, we should not expect the kind of neuronal decay and brain mass shrinkage that accompanies the third neurogenetic phase. Here are some genes associated with Alzheimer's Disease:
We all have APOE genes that direct the making of apolipoprotein E that forms lipoprotein molecules responsible for transporting cholesterol and other fats through the bloodstream. There are 3 different versions (alleles) of the APOE gene. The APOE-ε4 gene variant is the culprit for Alzheimer's risk. Approximately 25% of people carry one copy of this gene variant.
APP genes direct the making of amyloid precursor proteins located in the central nervous system's many tissues and organs. Enzymes cut off peptides and small fragments from the APPs, which then float outside of the cell. The enzymes are encoded by two genes presenilin 1 (PSEN1) and presenilin 2 (PSEN2) that mutate to cause Alzheimer's Disease.
TREM2 (triggering receptor expressed on myeloid cells 2)- mutations of this gene can cause Alzheimer's Disease. This gene is situated in cells crucial to hematopoiesis (blood cell formation) and the microglial cells crucial to central nervous system maintenance.
In conclusion:
The symptoms of Alzheimer's Disease (i.e., irremediable cognitive decline, memory deprivation, psychosis, hallucinations, and delusions) are the material manifestations of what is happening inside you. They humiliatingly steal away the most precious aspects of who you are. If there was anything immaterial inside us that was an eternal gift from an omnibenevolent divinity, we should expect it to at least protect who we are at the core. What is most sacred about us apparently cannot be protected from the ravages of life.
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