John K Grandy
Scientific Tracks Abstracts: J Neurol Neurophysiol
Alzheimer disease (AD) is a neurodegenerative disorder that slowly erodes some of the facets of human consciousness. During the pathological course of AD beta-amyloid plaques form which causes damage to neurons and results in the gross loss of brain volume. As a consequence of AD, the afflicted individual develops decreases in cognitive/executive function, memory, and the ability to inhibit inappropriate behaviors. Another way of saying this is that the afflicted individual ceases to be the person that they once were, i.e., their degree of consciousness has deteriorated. Mutations in several genes, e.g. APP, PSEN1, PSEN2, and TREM2; and the gene variant APOE-epsilon4, have been correlated to the development of AD. This has given support to the idea that there are neurogenetic correlates of consciousness (NgCC). In previous works these NgCC have been delineated into three neurogenetic phases of human consciousness. AD is a primary example of gene-based neurodegeneration in the third neurogenetic phase. There is hope that symptoms of AD may be reversed with the development of novel genetic therapies. Some gene therapies are underway, e.g. FGF2, leptin, NEU1, and Klotho KL-VS gene therapies. If these gene therapies, or other genetic therapies, are successful in reversing some of the symptoms of AD, can they eventually be used to enhance human consciousness in individuals without AD?
