AI Article Synopsis
- The study investigates the relationship between traumatic brain injury (TBI) and Alzheimer's disease (AD) by comparing AD patients with and without a history of TBI, focusing on various biomarkers in their cerebrospinal fluid (CSF).
- Researchers found no significant differences in baseline CSF biomarker levels or cognitive decline between the two groups of AD patients, suggesting that TBI may not directly affect AD progression.
- However, TBI occurring more than five years prior was linked to higher levels of specific biomarkers (NPTX2 and a trend for SNAP25), indicating possible long-term synaptic dysfunction effects when TBI occurs before the onset of AD.
Article Abstract
Traumatic brain injury (TBI) and Alzheimer's disease (AD) have overlapping mechanisms but it remains unknown if pathophysiological characteristics and cognitive trajectories in AD patients are influenced by TBI history. Here, we studied AD patients (stage MCI or dementia) with TBI history (AD n=110), or without (AD, n=110) and compared baseline CSF concentrations of amyloid beta 1-42 (Aβ42), phosphorylated tau181 (pTau181), total tau, neurofilament light chain (NfL), synaptosomal associated protein-25kDa (SNAP25), neurogranin (Ng), neuronal pentraxin-2 (NPTX2) and glutamate receptor-4 (GluR4), as well as differences in cognitive trajectories using linear mixed models. Explorative, analyses were repeated within stratified TBI groups by TBI characteristics (timing, severity, number). We found no differences in baseline CSF biomarker concentrations nor in cognitive trajectories between AD and AD patients. TBI >5 years ago was associated with higher NPTX2 and a tendency for higher SNAP25 concentrations compared to TBI ≤ 5 years ago, suggesting that TBI may be associated with long-term synaptic dysfunction only when occurring before onset or in a pre-clinical disease stage of AD.
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| http://dx.doi.org/10.1016/j.neurobiolaging.2024.06.001 | DOI Listing |
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