I was going to write this at some point after Alan put a link to the below Guardian article in the last post discussion, but someone else has asked me to post on it, so here we go.
I recently started work in Alzheimer’s for a Biotech that has a program in developing treatments for Alzheimer’s Disease (AD). As with all my work over the years in different diseases, I collaborate with leading academics and physicians in the disease area to develop research ideas – our own and theirs; discuss and disseminate latest research information and help facilitate the implementation of improved diagnostics and treatment pathways. I love what I do, whether it is in HIV, which I spent many years working in, or AD, which I have a particular passion for due to watching my father succumb to this hideous disease. The idea that I may be a part of helping deliver the first wave of potentially disease modifying therapies that slow the progress of this monstrous disease is hugely exciting.
Above is a picture of a normal brain and a brain that has been severely damaged due to AD . The brain of someone who dies with AD can weigh as much as 30% less than a normal brain at death. AD destroys the brain through a pathway that is widely understood to involve the deposition of Beta-Amyloid plaques in the neurons of the brain, which then through an immune response causes another protein called Tau, which has structural and metabolic roles in the neuron, to become dissociated with the neuron and eventually form clumps and neuronal death. This is the Amyloid cascade pathway that most scientists believe is the primary mechanism by which AD occurs. The process can start up to 20 years before symptoms appear, and once symptoms appear will usually kill the patient within 6-15 years. It is a terminal disease.
As the disease progresses patients go from experiencing mild cognitive impairment (MCI) which usually involves short term memory issues, to mild dementia which may affect one’s ability to do complex tasks, through to severe or advanced dementia where the patient is normally incapable of the most basic of tasks, becomes completely incontinent, and has lost all memory function or ability to speak. They are barely conscious as we understand consciousness. The final stage is death when the part of the brain that controls vital functions such as metabolism or heart rate etc becomes affected. Often dementia patients will die of chest infections as they lose their cough reflex and they literally drown in the fluid accumulating in their lungs. Often they will have pneumonia on their death certificates, but ultimately it is AD that killed them. In the UK it is now acknowledged as the biggest killer (over 20% of “with COVID” deaths are dementia patients). Suffice to say, at this stage the brain should not be functionally capable of lucidity.
Terminal, or paradoxical lucidity, is the phenomenon in which patients who have advanced AD and who have been in a state of cognitive non existence for months suddenly appear completely lucid or “their old selves again”. This usually occurs shortly before their deaths. It is not unique to AD patients, but from a scientific and philosophical perspective it is this group of patients that are most interesting and where those who have an interest in NDEs become excited.
Ultimately, terminal or paradoxical lucidity is not understood from a scientific perspective. A brain that has lost so much of its physical structure that the patient long ago lost cognitive function, and can no longer perform basic physiological functions like bladder control, should not be capable of “producing” high level conscious activity. It is a paradox, hence the alternative nomenclature. The overlap with NDEs, and hence the reason that Sam Parnia has become involved in this work, is obvious: people who report NDEs are reporting consciousness when the brain is completely incapable of consciousness from a scientific perspective because it is completely inactive.
The justification for research into this area is that maybe by understanding what activity we observe on an EEG during one of these terminal lucidity episodes, we may be able to develop technology that generates sufficient targeted stimulation to cause patients with AD to recover some of their function. There is a precedent for this. Currently available symptomatic treatments of AD, such as Donepezil, which slow the breakdown of the neurotransmitter acetyl choline, have been shown to improve cognitive function in some patients with AD, especially when used early. However these drugs do not alter the underlying disease process, they just “make better use of” the undamaged part of the brain; the patient will die at the same point with or without treatment. It is just a brain booster (student doctors have used it in medical exams to enhance their performance!). Arguably, if we can understand the physiological processes that are occurring during terminal lucidity, maybe we can devise technology that creates the same effect. That at least is the materialistic justification for this research.
Non-materialists, or “Nutters”, like me have a different explanation. The long established guest of the brain (the consciousness) has returned and somehow is able sequester the remnants of its dying host to experience and communicate with this realm one last time. It is a “paranormal” or “supernatural” phenomenon.