Abstract
Growth-associated protein 43 (GAP-43) is found in the axonal terminal of neurons in the limbic system, which is affected in people with Alzheimer's disease (AD). We assumed GAP-43 may contribute to AD progression and serve as a biomarker. So, in a two-year follow-up study, we assessed GAP-43 changes and whether they are correlated with tensor-based morphometry (TBM) findings in patients with mild cognitive impairment (MCI). We included MCI and cognitively normal (CN) people with available baseline and follow-up cerebrospinal fluid (CSF) GAP-43 and TBM findings from the ADNI database. We assessed the difference between the two groups and correlations in each group at each time point. CSF GAP-43 and TBM measures were similar in the two study groups in all time points, except for the accelerated anatomical region of interest (ROI) of CN subjects that were significantly greater than those of MCI. The only significant correlations with GAP-43 observed were those inverse correlations with accelerated and non-accelerated anatomical ROI in MCI subjects at baseline. Plus, all TBM metrics decreased significantly in all study groups during the follow-up in contrast to CSF GAP-43 levels. Our study revealed significant associations between CSF GAP-43 levels and TBM indices among people of the AD spectrum.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.