Medin synergized with vascular amyloid-beta deposits accelerates cognitive decline in Alzheimer's disease:a potential biomarker

Brain vascular dysfunction in Alzheimer s disease(AD) pathogenesis has become increasingly clea r.Accumulating evidence shows that damaged vascular,including large or small vessels and even neurovascular unit,may accelerate the neuropathological process of AD via disrupting brain hypoperfusion,aberrant angiogenesis,and neuroinflammatory response,etc.Thus,vascular dysfunction makes a substantially contribution to the cognitive decline of AD patients.

Artificial Immune Detection for Network Intrusion Data Based on Quantitative Matching Method

Artificial immune detection can be used to detect network intrusions in an adaptive approach and proper matching methods can improve the accuracy of immune detection methods.This paper proposes an artificial immune detection model for network intrusion data based on a quantitative matching method.The proposed model defines the detection process by using network data and decimal values to express features and artificial immune mechanisms are simulated to define immune elements.Then,to improve the accuracy of similarity calculation,a quantitative matching method is proposed.The model uses mathematical methods to train and evolve immune elements,increasing the diversity of immune recognition and allowing for the successful detection of unknown intrusions.The proposed model’s objective is to accurately identify known intrusions and expand the identification of unknown intrusions through signature detection and immune detection,overcoming the disadvantages of traditional methods.The experiment results show that the proposed model can detect intrusions effectively.It has a detection rate of more than 99.6%on average and a false alarm rate of 0.0264%.It outperforms existing immune intrusion detection methods in terms of comprehensive detection performance.

Vitamin D-binding protein in plasma microglia-derived extracellular vesicles as a potential biomarker for major depressive disorder

No well-established biomarkers are available for the clinical diagnosis of major depressive disorder(MDD).Vitamin D-binding protein(VDBP)is altered in plasma and postmortem dorsolateral prefrontal cortex(DLPFC)tissues of MDD patients.Thereby,the role of VDBP as a potential biomarker of MDD diagnosis was further assessed.Total extracellular vesicles(EVs)and brain cell-derived EVs(BCDEVs)were isolated from the plasma of first-episode drug-naïve or drug-free MDD patients and well-matched healthy controls(HCs)in discovery(20 MDD patients and 20 HCs)and validation cohorts(88 MDD patients and 38 HCs).VDBP level in the cerebrospinal fluid(CSF)from chronic glucocorticoid-induced depressed rhesus macaques or prelimbic cortex from lipopolysaccharide(LPS)-induced depressed mice and wild control groups was measured to evaluate its relationship with VDBP in plasma microglia-derived extracellular vesicles(MDEVs).VDBP was significantly decreased in MDD plasma MDEVs compared to HCs,and negatively correlated with HAMD-24 score with the highest diagnostic accuracy among BCDEVs.VDBP in plasma MDEVs was decreased both in depressed rhesus macaques and mice.A positive correlation of VDBP in MDEVs with that in CSF was detected in depressed rhesus macaques.VDBP levels in prelimbic cortex microglia were negatively correlated with those in plasma MDEVs in depressed mice.The main results suggested that VDBP in plasma MDEVs might serve as a prospective candidate biomarker for MDD diagnosis.

White matter microstructure mediates the pairwise relationship between childhood maltreatment,microRNA-9,and the severity of major depressive disorder

To the Editor:Major depressive disorder(MDD)affects over 300 million individuals globally,impairing daily life and leading to severe cases of suicide.Child maltreatment(CM),encompassing various types of mistreatment to children under 18 years,is a predisposing factor for MDD,with approximately 46%of MDD patients having experienced CM.[1]Understanding the biological mechanisms linking CM to MDD may reveal prevention and management strategies.

Waking Up Brain with Electrical Stimulation to Boost Memory in Sleep:A Neuroscience Exploration

Imagine that,in the future,you could enhance your memory by applying a mild electric current to your brain during sleep.This might sound like science fiction,but it is based on cutting-edge neuroscience research.Sleep is widely recognized as a crucial factor for long-term memory consolidation,but the exact mechanisms by which the brain coordinates neural activity across different regions during sleep to reorganize and integrate memories are unknown[1,2].

Peripheral ApoE4 Leads to Cerebrovascular Dysfunction and Aβ Deposition in Alzheimer's Disease

Alzheimer's disease(AD)is a neurodegenerative disease characterized by progressive cognitive dysfunction and behavioral impairment that occurs in old age and pre-old age[1].Apolipoprotein4(ApoE4)is the most important genetic risk factor for late-onset AD[2].Peripheral apoE4 is separated from that in the CNS by the blood-brain barrier(BBB)and is abundantly produced by the liver and macrophages and released into the blood to modulate lipid-related events.

Apolipoprotein E Drives Early Blood–Brain Barrier Damage in Alzheimer’s Disease

Recently,the essential functions of the blood-brain barrier(BBB)have attracted increasing attention in the pathophysiology of Alzheimer's disease(AD)[1].How apolipoprotein E(APOE4),the most important high-risk gene for late-onset AD[2],drives early BBB damage in AD patients remains unclear.