Traumatic Brain Injury and Alzheimer’s Disease: A Shared Neurovascular Hypothesis DOI Creative Commons

Gabrielle Cognacq,

Jonathan E. Attwood, Gabriele C. DeLuca

et al.

Neuroscience Insights, Journal Year: 2025, Volume and Issue: 20

Published: Feb. 1, 2025

Traumatic brain injury (TBI) is a modifiable risk factor for Alzheimer’s disease (AD). TBI and AD share several histopathological hallmarks: namely, beta-amyloid aggregation, tau hyperphosphorylation, plasma protein infiltration. The relative contributions of these proteinopathies their interplay in the pathogenesis both conditions remains unclear although important differences are emerging. This review synthesises emerging evidence critical role neurovascular unit mediating accumulation neurotoxicity AD. We propose shared pathogenic cascade centred on unit, which increased blood-brain barrier permeability induces series noxious mechanisms leading to neuronal loss, synaptic dysfunction ultimately cognitive conditions. explore application this hypothesis outstanding research questions potential treatments AD, as well other neurodegenerative neuroinflammatory Limitations hypothesis, including challenges establishing causal relationship between damage proteinopathies, also discussed.

Language: Английский

Identification of Key Fatty Acid Metabolism-Related Genes in Alzheimer’s Disease DOI
Bo Yan, Pan Liao, Wei Zhang

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: March 19, 2025

Language: Английский

Citations

0
Evaluating the Link Between Cardiovascular Risk and Alzheimer’s Disease: A Comprehensive Case-Control Study in Castilla y León, Spain DOI Creative Commons
Laura Bello-Corral, Jesús Seco‐Calvo,

Marta Celorrio San Miguel

et al.

Applied Sciences, Journal Year: 2025, Volume and Issue: 15(6), P. 3409 - 3409

Published: March 20, 2025

Alzheimer’s disease (AD) represents a growing public health challenge due to its increasing prevalence, projected reach 150 million cases by 2050. Characterised neuropathological changes such as the accumulation of beta-amyloid peptide and hyperphosphorylated Tau protein, is related genetic environmental factors. The main objective this research has been analyse possible relationship between some cardiovascular factors AD. This analytical observational case-control study carried out in Castilla y León (Spain), comprised total 511 individuals 60 90 years age, whom 260 had diagnosis AD rest were healthy individuals. results showed that group with predominantly women, widowed primary education, who higher prevalence family history disease. It was also observed hypertension, cardiac pathology diabetes mellitus three risk significant increased differences patients compared control Although precise mechanisms require further research, these underline importance addressing complex interactions prevention

Language: Английский

Citations

0
Traumatic Brain Injury and Alzheimer’s Disease: A Shared Neurovascular Hypothesis DOI Creative Commons

Gabrielle Cognacq,

Jonathan E. Attwood, Gabriele C. DeLuca

et al.

Neuroscience Insights, Journal Year: 2025, Volume and Issue: 20

Published: Feb. 1, 2025

Traumatic brain injury (TBI) is a modifiable risk factor for Alzheimer’s disease (AD). TBI and AD share several histopathological hallmarks: namely, beta-amyloid aggregation, tau hyperphosphorylation, plasma protein infiltration. The relative contributions of these proteinopathies their interplay in the pathogenesis both conditions remains unclear although important differences are emerging. This review synthesises emerging evidence critical role neurovascular unit mediating accumulation neurotoxicity AD. We propose shared pathogenic cascade centred on unit, which increased blood-brain barrier permeability induces series noxious mechanisms leading to neuronal loss, synaptic dysfunction ultimately cognitive conditions. explore application this hypothesis outstanding research questions potential treatments AD, as well other neurodegenerative neuroinflammatory Limitations hypothesis, including challenges establishing causal relationship between damage proteinopathies, also discussed.

Language: Английский

Citations

0