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Numrering	Referens	Omslagsbild	Hitta
1.	Ramos-Cejudo, J., et al. (författare) Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link 2018 Ingår i: EBioMedicine. - : Elsevier BV. - 2352-3964. ; 28, s. 21-30 Tidskriftsartikel (refereegranskat)abstract Traumatic brain injury (TBI) and Alzheimer's disease (AD) are devastating neurological disorders, whose complex relationship is not completely understood. Cerebrovascular pathology, a key element in both conditions, could represent amechanistic link between A beta/tau deposition after TBI and the development of post concussive syndrome, dementia and chronic traumatic encephalopathy (CTE). In addition to debilitating acute effects, TBI-induced neurovascular injuries accelerate amyloid beta (A beta) production and perivascular accumulation, arterial stiffness, tau hyperphosphorylation and tau/A beta-induced blood brain barrier damage, giving rise to a deleterious feed-forward loop. We postulate that TBI can initiate cerebrovascular pathology, which is causally involved in the development of multiple forms of neurodegeneration including AD-like dementias. In this review, we will explore hownovel biomarkers, animal and human studies with a focus on cerebrovascular dysfunction are contributing to the understanding of the consequences of TBI on the development of AD-like pathology.

Ramos-Cejudo, J., et al. (författare)
Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link
2018
Ingår i: EBioMedicine. - : Elsevier BV. - 2352-3964. ; 28, s. 21-30
Tidskriftsartikel (refereegranskat)abstract
- Traumatic brain injury (TBI) and Alzheimer's disease (AD) are devastating neurological disorders, whose complex relationship is not completely understood. Cerebrovascular pathology, a key element in both conditions, could represent amechanistic link between A beta/tau deposition after TBI and the development of post concussive syndrome, dementia and chronic traumatic encephalopathy (CTE). In addition to debilitating acute effects, TBI-induced neurovascular injuries accelerate amyloid beta (A beta) production and perivascular accumulation, arterial stiffness, tau hyperphosphorylation and tau/A beta-induced blood brain barrier damage, giving rise to a deleterious feed-forward loop. We postulate that TBI can initiate cerebrovascular pathology, which is causally involved in the development of multiple forms of neurodegeneration including AD-like dementias. In this review, we will explore hownovel biomarkers, animal and human studies with a focus on cerebrovascular dysfunction are contributing to the understanding of the consequences of TBI on the development of AD-like pathology.

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