Introduction: Blood-brain barrier (BBB) breakdown is observed in older versus younger adults and in late-onset Alzheimer's disease versus age-matched controls, but its causes and consequences in aging are unclear. We tested the hypothesis that BBB breakdown is associated with cognitive decline and inflammation in nondemented elders.
Methods: Cerebrospinal fluid and serum inflammatory markers were measured using sandwich immunoassays in 120 subjects. Least Absolute Shrinkage and Selection Operator-logistic regression selected cerebrospinal fluid and serum signatures that best classified BBB impairment defined by the cerebrospinal fluid albumin index ≥9. Linear regression examined changes in Clinical Dementia Rating sum of boxes as a function of BBB integrity at baseline.
Results: Mean age was 70 years, mean Mini–Mental State Examination was 27, and BBB impairment was recorded in 13.5%. BBB breakdown was associated with cognitive decline (P = .015). Cerebrospinal fluid intercellular adhesion molecule-1, vascular endothelial growth factor, interleukin-8, serum amyloid A, macrophage derived chemokine, and gender generated an area under the curve of 0.95 for BBB impairment, and serum IL-16, VEGF-D, IL-15, and other variables generated an AUC of 0.92 for BBB impairment.
Discussion: BBB breakdown is associated with more rapid cognitive decline. Inflammatory mechanisms, including cell adhesion, neutrophil migration, lipid metabolism, and angiogenesis may be implicated.
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http://dx.doi.org/10.1016/j.jalz.2018.06.2857 | DOI Listing |
Alzheimers Res Ther
January 2025
Department of Radiology, Weill Medical College of Cornell University, New York, NY, USA, Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
Background: Quantitative susceptibility mapping (QSM) can study the susceptibility values of brain tissue which allows for noninvasive examination of local brain iron levels in both normal and pathological conditions.
Purpose: Our study compares brain iron deposition in gray matter (GM) nuclei between cerebral small vessel disease (CSVD) patients and healthy controls (HCs), exploring factors that affect iron deposition and cognitive function.
Materials And Methods: A total of 321 subjects were enrolled in this study.
Fluids Barriers CNS
January 2025
Sanders-Brown Center on Aging, College of Medicine, University of Kentucky, 760 Press Ave, 124 HKRB, Lexington, KY, 40536-0679, USA.
Background: Blood-brain barrier dysfunction is one characteristic of Alzheimer's disease (AD) and is recognized as both a cause and consequence of the pathological cascade leading to cognitive decline. The goal of this study was to assess markers for barrier dysfunction in postmortem tissue samples from research participants who were either cognitively normal individuals (CNI) or diagnosed with AD at the time of autopsy and determine to what extent these markers are associated with AD neuropathologic changes (ADNC) and cognitive impairment.
Methods: We used postmortem brain tissue and plasma samples from 19 participants: 9 CNI and 10 AD dementia patients who had come to autopsy from the University of Kentucky AD Research Center (UK-ADRC) community-based cohort; all cases with dementia had confirmed severe ADNC.
Sci Rep
January 2025
Department of Neurology, Neurological Institute, Taichung Veterans General Hospital, No. 1650, Taiwan Boulevard, Section 4, Taichung, 40705, Taiwan.
This study investigates whether incorporating olfactory dysfunction into motor subtypes of Parkinson's disease (PD) improves associations with clinical outcomes. PD is commonly divided into motor subtypes, such as postural instability and gait disturbance (PIGD) and tremor-dominant PD (TDPD), but non-motor symptoms like olfactory dysfunction remain underexplored. We assessed 157 participants with PD using the University of Pennsylvania Smell Identification Test (UPSIT), Movement Disorder Society-Sponsored Revision of the Unified Parkinson's Disease Rating Scale (M-UPDRS), Montreal Cognitive Assessment (MoCA), 39-item Parkinson's Disease Questionnaire Summary Index (PDQ-39 SI), and 99mTc-TRODAT-1 imaging.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Psychiatry and Behavioral Sciences, School of Medicine, Stanford University, 401 Quarry Road, Stanford, CA, 94305, USA.
Background: Intermittent hypoxia, a consequence of sleep-disordered breathing (SDB), may contribute to an increased risk of cognitive decline. However, the association between SDB and cognition remains highly variable.
Methods: Fifty-two community-dwelling healthy older adults (28 women) were recruited.
Nat Commun
January 2025
China CDC Key Laboratory of Environment and Population Health, National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing, China.
It remains unclear whether the benefits of adhering to a healthy lifestyle outweigh the effects of high genetic risk on cognitive decline. We examined the association of combined lifestyle factors and genetic risk with changes in cognitive function and six specific dimensions of cognition among older adults from the Chinese Longitudinal Healthy Longevity Survey (1998-2018, n = 18,811, a subset of 6301 participants with genetic information). Compared to participants with an unfavorable lifestyle, those with a favorable lifestyle showed a 46.
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