Plasma S100β is a predictor for pathology and cognitive decline in Alzheimer’s disease

Fluids and Barriers of the CNS, Journal Year: 2025, Volume and Issue: 22(1)

Published: Jan. 9, 2025

Blood–brain barrier dysfunction is one characteristic of Alzheimer's disease (AD) and recognized as both a cause consequence the pathological cascade leading to cognitive decline. The goal this study was assess markers for in postmortem tissue samples from research participants who were either cognitively normal individuals (CNI) or diagnosed with AD at time autopsy determine what extent these are associated neuropathologic changes (ADNC) impairment. We used brain plasma 19 participants: 9 CNI 10 dementia patients had come University Kentucky Research Center (UK-ADRC) community-based cohort; all cases confirmed severe ADNC. Plasma obtained within 2 years autopsy. Aβ40, Aβ42, tau levels quantified by ELISA. Cortical sections cleared using X-CLARITY™ system immunostained neurovascular unit-related proteins. Brain slices then imaged confocal microscopy analyzed microvascular diameters immunoreactivity coverage Fiji/ImageJ. Isolated human microvessels assayed tight-junction protein expression JESS™ automated Western blot system. S100 calcium-binding B (S100β), matrix metalloproteinase (MMP)-2, MMP-9, neuron-specific enolase (NSE) All outcomes assessed linear associations global function (MMSE, CDR) cerebral atrophy scores Pearson, polyserial, polychoric correlation, appropriate, along generalized modeling mixed-level modeling. As expected, we detected elevated Aβ pathology compared CNI. However, found no differences sections. also observed claudin-5 capillaries isolated samples. biomarker analysis showed that 12.4-fold higher S100β levels, twofold lower NSE 2.4-fold MMP-9 1.2-fold MMP-2 than Data revealed predictive Our data suggest among different relevant dysfunction, most promising diagnostic Further investigation necessary how relate whether they may predict clinical outcomes, particularly prodromal early stages AD.

Language: Английский

Platycodin D and voluntary running synergistically ameliorate memory deficits in 5 × FAD mice via mediating neuromodulation and neuroinflammation

Frontiers in Aging Neuroscience, Journal Year: 2024, Volume and Issue: 16

Published: Sept. 25, 2024

Alzheimer's disease (AD) is the leading cause of dementia, and currently, no effective treatments are available to reverse or halt its progression in clinical practice. Although a plethora studies have highlighted benefits physical exercise combating AD, elder individuals often limited capacity. Therefore, mild nutritional interventions represent potential strategies for preventing mitigating neurodegenerative diseases. Our research, along with other studies, demonstrated that platycodin D (PD) metabolite, platycodigenin, derived from medicinal plant

Language: Английский