Skip to main content

Open Access Abstracts for the 17th Annual Meeting of the American Society for Neural Therapy and Repair

Download Article:
(HTML 5,317.2 kb)
(PDF 303 kb)
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).
No References for this article.
No Supplementary Data.
No Article Media
No Metrics

Document Type: Abstract

Affiliations: 1: , Cardiff, South Wales, 2: , Minneapolis, MN, 3: , Denver, CO,

Publication date: 01 March 2010

More about this publication?
  • Cell Transplantation publishes original, peer-reviewed research and review articles on the subject of cell transplantation and its application to human diseases. To ensure high-quality contributions from all areas of transplantation, separate section editors and editorial boards have been established. Articles deal with a wide range of topics including physiological, medical, preclinical, tissue engineering, and device-oriented aspects of transplantation of nervous system, endocrine, growth factor-secreting, bone marrow, epithelial, endothelial, and genetically engineered cells, among others. Basic clinical studies and immunological research papers are also featured. To provide complete coverage of this revolutionary field, Cell Transplantation will report on relevant technological advances, and ethical and regulatory considerations of cell transplants. Cell Transplantation is now an Open Access journal starting with volume 18 in 2009, and therefore there will be an inexpensive publication charge, which is dependent on the number of pages, in addition to the charge for color figures. This will allow work to be disseminated to a wider audience and also entitle the corresponding author to a free PDF, as well as prepublication of an unedited version of the manuscript.

    Cell Transplantation is now being published by SAGE. Please visit their website for the most recent issues.

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more