2025/03/26 by Bryan Sun, Lulin Li, Odette A. Harris +1 · 1 voice · 27 citations
Biochemistry, Genetics and Molecular Biology · Medicine · Neuroscience · Psychology · #Blood–brain barrier #Central nervous system #Disease #Medicine #Mitochondrial Function and Pathology #Neurodegeneration #Neurology #Neuroscience #Pathological #Pathology #Psychiatry #Psychology #Traumatic Brain Injury Research #Traumatic Brain Injury and Neurovascular Disturbances #Traumatic brain injury
paper · pdf · doi:10.1186/s40035-025-00478-5
published in Translational Neurodegeneration 14(1), 16 (BioMed Central)
openalex publication_date 2025/03/26 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29
Traumatic brain injury (TBI) has emerged as a significant risk factor for Alzheimer's disease (AD), a complex and devastating neurodegenerative disorder characterized by progressive cognitive decline and memory loss. Both conditions share a common feature: blood‒brain barrier (BBB) dysfunction, which is believed to play a pivotal role in linking TBI to the development of AD. This review delves into the intricate relationship between TBI and AD, with a focus on BBB dysfunction and its critical role in disease mechanisms and therapeutic development. We first present recent evidence from epidemiological studies highlighting the increased incidence of AD among individuals with a history of TBI, as well as pathological and animal model studies that demonstrate how TBI can accelerate AD-like pathology. Next, we explore the mechanisms by which BBB dysfunction may mediate TBI-induced AD pathology. Finally, we investigate the shared molecular pathways associated with BBB dysfunction in both TBI and AD conditions and discuss the latest findings on how targeting these pathways and employing regenerative approaches, such as stem cell therapy and pharmacological interventions, can enhance BBB function and mitigate neurodegeneration.