Conclusions
ARHL is a complex disorder, influenced by genetic,
environmental/lifestyle and stochastic factors. Despite
its high prevalence and the recent progress in hear-
ing research, few attempts to identify genetic deter-
minants of ARHL have been made. In this post-
genome era, with high-throughput genotyping plat-
forms now developed, a HapMap project to guide
marker selection, the constructive challenge we face
is to find strategies that are best suited to unravel
the genetic basis of complex traits such as presbyscu-
sis. The reverse genetics approach, where phenotypes
are refined in relation to genetic marker data (linkage
and linkage-disequilibrium analysis), although statis-
tical challenges remain, may lead to the identifica-
tion of susceptibility components for ARHL. On the other hand, forward genetics may also be a promis-
ing approach. Isolating all the genes in the human
genome, as well as identifying and cataloguing the
functional variants within them in the human popula-
tion, will allow assessment of the impact of genotype
on phenotypic outcome of interest. Additionally, com-
plementary strategies, based on functional genomics
technology involving microarrays and proteomics, can
be used to develop predictors of disease susceptibility
based on biological pathways physiologically relevant
to ARHL. Nevertheless, choices in study designs will
still be the major factor in the probability of suc-
cess. Determination of the genetic variants involved
in ARHL should provide new insights into the dis-
order mechanism, which may uncover new leads for
pharmaceutical intervention and could result in the
development of screening kits to identify individuals
at increased risk.