BMC neurology · 2025
Growth associated protein 43 (GAP-43) predicts brain amyloidosis in Alzheimer's dementia continuum: an [18 F] AV-45 study.
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Nemati Rezvan, Sohrabi-Ashlaghi Ahmadreza, Saberian Parsa, Sadeghi Mohammad, Mardani Sajjad, Abadi Amir Sina Jafari Hossein, Yaghoobpoor Ali, Heydari Atefeh, Khoshroo Niloofar, Rahnama Yassin, Mayeli Mahsa, Nasiri Hamide
Аннотация
BACKGROUND: Growth-associated protein 43 (GAP-43) is a key protein involved in neuronal growth and synaptic plasticity. Alterations in GAP-43 levels have been associated with Alzheimer's Disease (AD), potentially reflecting synaptic dysfunction. We evaluated the potential of GAP-43 as a biomarker for AD and explored its association with amyloid-beta (Aβ) levels, as well as its correlation with Aβ plaque burden in the brain.
METHODS: We screened 1,639 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. A total of 226 individuals met the eligibility criteria and were enrolled. Participants were classified into three groups: 77 cognitively normal (CN) individuals, 111 with mild cognitive impairment (MCI), and 38 with a diagnosis of AD. The associations between cerebrospinal fluid (CSF) GAP-43 levels with other biomarkers as well as [¹⁸F] AV-45 (Florbetapir) PET Standardized Uptake Value Ratios (SUVR) were investigated.
RESULTS: Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups. Furthermore, GAP-43 levels showed a significant positive correlation with tau pathology. Notably, we observed a significant association between GAP-43 and [¹⁸F] Florbetapir PET SUVR in the MCI group, suggesting that GAP-43 may serve as a reliable biomarker in the early stages of AD.
CONCLUSION: This study provides evidence supporting the role of GAP-43 as a potential biomarker for AD, particularly in relation to predicting the amyloid pathology pattern in the brain in the MCI stage.
METHODS: We screened 1,639 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. A total of 226 individuals met the eligibility criteria and were enrolled. Participants were classified into three groups: 77 cognitively normal (CN) individuals, 111 with mild cognitive impairment (MCI), and 38 with a diagnosis of AD. The associations between cerebrospinal fluid (CSF) GAP-43 levels with other biomarkers as well as [¹⁸F] AV-45 (Florbetapir) PET Standardized Uptake Value Ratios (SUVR) were investigated.
RESULTS: Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups. Furthermore, GAP-43 levels showed a significant positive correlation with tau pathology. Notably, we observed a significant association between GAP-43 and [¹⁸F] Florbetapir PET SUVR in the MCI group, suggesting that GAP-43 may serve as a reliable biomarker in the early stages of AD.
CONCLUSION: This study provides evidence supporting the role of GAP-43 as a potential biomarker for AD, particularly in relation to predicting the amyloid pathology pattern in the brain in the MCI stage.