According to a recent hypothesis, neurodegenerative diseases are age-related diseases of specific brain regions that have developed relatively recently in evolutionary time in Homo sapiens (Ghika, 2008). Alzheimer's disease was the first to be thought of as a disease of “phylogenic regression” (Rapoport 1988, 1989), a concept comparing brain aging “involution” to the reversed phenomenon of darwinian evolution. There is recent scientific evidence that suggests that “premature aging” associated with neurodegeneration in humans involves phyllogenetically/evolutionarily recent cortical areas, that are more prone to cell death because of higher levels of plasticity due to more rapid evolution. It is hypothesized that premature aging of the “new” cortical areas may be due to ongoing evolution and as of yet “not fixed genome” in newly established cortical networks that have specific sensitivity to age and apoptosis, mutations, or loss of differentiation because of higher levels of plasticity and wider connections as secondary or integrative cortical areas (Ghika, 2008). These ideas are an intriguing way of thinking of neurodegenerative diseases; however, their validity remains to be determined. In the ASNTR Presidential Lecture for 2010, renowned human geneticist and molecular biologist Dr. John Hardy, UCL Institute of Neurology, London, will present a talk entitled “Whole Genome Analysis of Neurodegenerative Disease.” He will discuss genome-wide association studies and human disease genetic risk factors for neurologic diseases, highlighting in a portion of his talk evidence suggesting that Homo neanderthalensis contributed the H2 MAPT haplotype to Homo sapiens. The idea of paleoneurology may give a new perspective of seeing clinical signs in neurodegenerative diseases as “homo-specific syndromic presentations rather than patho-specific diseases“ (Ghika, 2008).
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Publication date: 01 March 2010
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