Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder characterized by aberrant amyloid precursor protein (APP) cleavage, pathological aggregations of beta-amyloid (Aβ) that make up Aβ plaques and hyperphosphorylation of Tau that makes up neurofibrillary tangles (NFTs). Although progress has been made in research on AD, the fundamental causes of this disease have not been fully elucidated. Recent studies have shown that vascular dysfunction especially the loss of pericytes plays a significant role in the onset of AD. Pericytes play a variety of important roles in the nervous system including the regulation of the cerebral blood flow (CBF), the formation and maintenance of the blood–brain barrier (BBB), angiogenesis, and the clearance of toxic substances from the brain. Pericytes participate in the transport of Aβ through various receptors, and Aβ acts on pericytes to cause them to constrict, detach, and die. The loss of pericytes elevates the levels of Aβ1-40 and Aβ1-42 by disrupting the integrity of the BBB and reducing the clearance of soluble Aβ from the brain interstitial fluid. The aggravated deposition of Aβ further exacerbates pericyte dysfunction, forming a vicious cycle. The combined influence of these factors eventually results in the loss of neurons and cognitive decline. Further exploration of the interactions between pericytes and Aβ is beneficial for understanding AD and could lead to the identification of new therapeutic targets for the prevention and treatment of AD. In this review, we explore the characterization of pericytes, interactions between pericytes and other cells in the neurovascular unit (NVU), and the physiological functions of pericytes and dysfunctions in AD. This review discusses the interactions between pericytes and Aβ, as well as current and further strategies for preventing or treating AD targeting pericytes.

Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is primary in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transforma

Neuroinflammation may be involved in the pathogenesis of idiopathic normal pressure hydrocephalus (iNPH). However, the specific changes in the peripheral inflammatory state of patients with iNPH remain unclear. To explore the changes in the peripheral inflammatory state of patients with iNPH and their potential value as biomarkers of clinical diagnosis and disease severity. In this cross-sectional study, 119 iNPH patients with AD-negative pathology and 200 healthy controls (HCs) were enrolled. Clinical characteristics, including the Idiopathic Normal Pressure Hydrocephalus Grading Scale (iNPHGS), Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA), were collected along with inflammatory parameters in the peripheral blood. Logistic regression was applied to evaluate differences in peripheral inflammatory indicators, adjusting for age, sex, and comorbidities. Receiver operating characteristic (ROC) analysis was used to evaluate the diagnostic performance of the inflammatory markers. Correlations between inflammatory parameters and clinical characteristics were assessed. Significant differences in inflammatory parameters, such as neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and prognostic nutritional index (PNI), were observed between iNPH patients and HCs after adjusting for age, sex and comorbidities. The combination of PNI and platelet-to-high-density lipoprotein ratio (PHR) distinguished iNPH patients from HCs most significantly (area under the curve [AUC] = 0.820). Neutrophil ratio and lymphocyte ratio were associated with clinical severity and cognitive impairment of patients with iNPH. iNPH patients exhibit an elevated peripheral inflammatory state. Peripheral inflammatory parameters, especially neutrophil ratio and lymphocyte ratio, are associated with disease severity and cognitive impairment, suggesting their potential as therapeutic targets and offering new insights into the pathophysiology of iNPH. Additionally, the inflammatory peripheral parameters may serve as valuable and convenient method in assisting clinical diagnosis.