For fans of the Hameroff-Penrose
microtubule theory of consciousness (which hypothesizes that consciousness arises from quantum processes occurring within the
microtubules found in every neuron and cell):
Hameroff et al published a
paper not so long ago hypothesizing that a degradation in microtubule polymerization and stability leads to the reduction of conscious awareness, memory and cognitive function that is characteristic of Alzheimer's, proposing that microtubules are destabilized as a result of altered intracellular zinc levels (the zinc levels are themselves perturbed by the beta amyloid plaque found in Alzheimer's).
In the Hameroff-Penrose theory, microtubules are posited to be the fundamental organelles which generate consciousness from quantum processes (the hollow interiors of microtubules are thought to be so well protected from thermal noise that they can successfully host the incredibly delicate quantum waves).
If this theory of consciousness is true, you might expect consciousness to begin to fail when these microtubules become unstable.
Tau and
MAP2 are two very important proteins that stabilize microtubules in neurons, so if these proteins become defective, this may affect the microtubules. In the above-cited paper, the Hameroff et al propose that altered intracellular zinc levels result in defective tau protein being produced, leading to microtubule instability, when then results in all the problems with consciousness, memory and cognitive function you find in Alzheimer's.
It's early days yet, but Alzheimer's might turn out to provide evidence for the Hameroff-Penrose theory of consciousness.
All this might also have some import for ME/CFS: since the brain fog of ME/CFS feels like you have a deficit of consciousness, I was looking to see if anything in the pathophysiology of ME/CFS might perturb microtubule stability, and thereby contribute to the zombie-like state that we know as brain fog.
Interestingly enough, I found
one study which showed
ME/CFS patients have higher levels of autoantibodies to the MAP2 protein.
Another study found the same thing in lupus patients, and noted that lupus patients with anti-MAP2 autoantibodies were more likely to have neuropsychiatric symptoms such as psychosis, seizure, neuropathy, and cerebritis.