Reduced cerebrovascular response to neuronal activation is observed in patients with neurodegenerative disease. In the present study, we examined the correlation between reduced cerebrovascular response to visual activation (ΔCBF) and subclinical cognitive deficits in a human population of mid-sixties individuals without neurodegenerative disease. Such a correlation would suggest that impaired cerebrovascular function occurs before overt neurodegenerative disease. A total of 187 subjects (age 64-67 years) of the Metropolit Danish Male Birth Cohort participated in the study. ΔCBF was measured using arterial spin labelling (ASL) MRI. ΔCBF correlated positively with cognitive performance in: Global cognition (p = 0.046), paired associative memory (p = 0.025), spatial recognition (p = 0.026), planning (p = 0.016), simple processing speed (p < 0.01), and with highly significant correlations with current intelligence (p < 10), and more complex processing speed (p < 10), the latter two explaining approximately 11-13% of the variance. Reduced ΔCBF was independent of brain atrophy. Our findings suggest that inhibited cerebrovascular response to neuronal activation is an early deficit in the ageing brain and associated with subclinical cognitive deficits. Cerebrovascular dysfunction could be an early sign of a trajectory pointing towards the development of neurodegenerative disease. Future efforts should elucidate if maintenance of a healthy cerebrovascular function can protect against the development of dementia.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617000 | PMC |
http://dx.doi.org/10.1007/s11357-022-00596-2 | DOI Listing |
Mol Med Rep
March 2025
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, SAR 999078, P.R. China.
Subarachnoid hemorrhage (SAH), a prevalent cerebrovascular condition associated with a high mortality rate, frequently results in neuronal apoptosis and an unfavorable prognosis. The adjunctive use of traditional Chinese medicine (TCM) with surgical interventions exerts a therapeutic impact on SAH, potentially by facilitating apoptosis. However, the mechanism by which TCM mediates apoptosis following SAH remains unclear.
View Article and Find Full Text PDFActa Neurochir (Wien)
January 2025
Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 110 Francis Street , Boston, MA, 02215, USA.
Background: Variability in long-term endovascular treatment outcomes for intracranial aneurysms has prompted questions regarding the effects of these treatments on aneurysm hemodynamics. Endovascular techniques disrupt aneurysmal blood flow and shear, but their influence on intra-aneurysmal pressure remains unclear. A better understanding of aneurysm pressure effects may aid in predicting outcomes and guiding treatment decisions.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Institute of Physiology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address:
Background: Fabry disease (FD) patients are known to be at high risk of developing neuropsychiatric symptoms such as anxiety, depression and cognitive deficits. Despite this, they are underdiagnosed and inadequately treated. It is unknown whether these symptoms arise from pathological glycosphingolipid deposits or from cerebrovascular abnormalities affecting neuronal functions in the central nervous system.
View Article and Find Full Text PDFNeuron
January 2025
Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA. Electronic address:
As global life expectancy increases, age-related brain diseases such as stroke and dementia have become leading causes of death and disability. The aging of the neurovasculature is a critical determinant of brain aging and disease risk. Neurovascular cells are particularly vulnerable to aging, which induces significant structural and functional changes in arterial, venous, and lymphatic vessels.
View Article and Find Full Text PDFBackground: Vascular pathology associated with small vessel disease (SVD), such as microinfarcts and microbleeds, are common in elderly populations and significant contributors to cognitive impairment and dementia. Autosomal dominant cerebral arteriopathy with subcortical infarctions and leukoencephalopathy (CADASIL), caused by mutations in the Notch3 gene, is the most prominent inheritable SVD, with a common etiology of subcortical strokes and dementia. This study aimed to investigate additive or synergistic effects of CADASIL‐related vascular alterations and familial Alzheimer’s disease (FAD)‐related amyloid pathology on cerebral metabolism of glucose and disease progression in a novel FAD‐CADASIL mouse model.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!