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S5‐01‐02: C. elegans models of Alzheimer's disease and Parkinson's disease: Systems biology identifies LRRK2 shared interaction networks
Author(s) -
Wolozin Benjamin
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.517
Subject(s) - lrrk2 , gene knockdown , biology , caenorhabditis elegans , rna interference , genetics , context (archaeology) , gene , neurodegeneration , parkinson's disease , microbiology and biotechnology , rna , disease , mutation , pathology , medicine , paleontology
amyloid is being deposited in association cortex very early, usually several years before onset of clinical symptoms. Atrophy, predominantly of mesial temporal areas, and changes of white matter tracts are associated with onset of significant memory problems. Progressive dysfunction of cortical networks is then seen in FDG PET and fMRI studies, typically a few years before onset of dementia. Transmitter and receptor imaging by PET and SPECT relates cognitive impairment to specific neurotransmitter systems. The influence of age-at-onset, education, vascular changes, genetic factors and microglial activation is being studied, and imaging techniques are being evaluated as biomarkers for clinical trials aiming at prevention of dementia and reduction of disease progression. Conclusions: Molecular imaging confirms very early deposition of amyloid at a presymptomatic stage of AD, while further studies are underway to identify additional factors influencing progression to dementia.