Alzheimer’s disease (AD) and schizophrenia are traditionally considered distinct clinical entities, yet growing evidence highlights substantial overlap in their molecular and neuroinflammatory pathogenesis. This review explores current insights into the shared and divergent mechanisms underlying these disorders, with emphasis on neuroinflammation, autophagy dysfunction, blood–brain barrier (BBB) disruption, and cognitive impairment. We examine key signaling pathways, particularly spleen tyrosine kinase (SYK), the mechanistic (or mammalian) target of rapamycin (mTOR), and the S100 calcium-binding protein B (S100B)/receptor for advanced glycation end-products (RAGE) axis, that link glial activation, excitatory/inhibitory neurotransmitter imbalances, and impaired proteostasis across both disorders. Specific biomarkers such as S100B, matrix metalloproteinase 9 (MMP9), and soluble RAGE show promise for stratifying disease subtypes and predicting treatment response. Moreover, psychiatric symptoms frequently precede cognitive decline in both AD and schizophrenia, suggesting that mood and behavioral disturbances may serve as early diagnostic indicators. The roles of autophagic failure, cellular senescence, and impaired glymphatic clearance are also explored as contributors to chronic inflammation and neurodegeneration. Current treatments, including cholinesterase inhibitors and antipsychotics, primarily offer symptomatic relief, while emerging therapeutic approaches target upstream molecular drivers, such as mTOR inhibition and RAGE antagonism. Finally, we discuss the future potential of personalized medicine guided by genetic, neuroimaging, and biomarker profiles to optimize diagnosis and treatment strategies in both AD and schizophrenia. A greater understanding of the pathophysiological convergence between these disorders may pave the way for cross-diagnostic interventions and improved clinical outcomes.

C-reactive protein (CRP) has emerged as a crucial link between systemic and neuroinflammatory processes, though its role across neurological autoimmune disorders remains incompletely understood. Pathologies such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), Guillain–Barré syndrome (GBS), and myasthenia gravis (MG) share chronic, dysregulated inflammation resulting from loss of immune tolerance. Their pathogenesis arises from interactions among genetic susceptibility, environmental factors, and gut microbiota alterations that trigger autoreactive immune cascades through molecular mimicry, ectopic antigen expression, or paraneoplastic cross-reactivity. These immune pathways sustain inflammation and promote neuroaxonal injury. CRP, synthesized mainly by hepatocytes in response to interleukin-6 (IL-6), functions as both an effector and reporter of inflammation, linking systemic immune activation to neuroinflammatory damage. Elevated CRP levels correlate with unfavorable outcomes, including accelerated disability in MS, IL-6-mediated astrocyte injury in NMOSD, respiratory failure in GBS, and crisis susceptibility in MG. Composite indices such as the CRP-to-albumin ratio are emerging as refined prognostic markers, though interpretation is limited by non-specificity and biological variability. This review integrates current evidence on CRP’s mechanistic roles, clinical associations, and translational potential in neuroinflammatory disorders, combining molecular, clinical, and imaging perspectives to refine its role within inflammation-driven neurodegeneration.

Background: Obesity has emerged as a global pandemic, manifesting as metabolic, social, and psychological disorders. Traditional bariatric approaches have long been the cornerstone of obesity treatment; however, laparoscopic greater curvature plication (LGCP) has gained recognition as a viable, minimally invasive alternative. Aim of the study: The aim of this study is to evaluate the impact of LGCP on weight loss, obesity-related comorbidities, and quality of life in patients with a Body Mass Index (BMI) =35 kg/m². Materials and Methods: A retrospective analysis was conducted on 50 patients (45 women and 5 men) who underwent LGCP. The average preoperative BMI was 38.71 kg/m². Inclusion criteria targeted patients with a BMI =35 kg/mò with obesity-related comorbidities or =40 kg/m² regardless of comorbidity status. Preoperative and postoperative data collection included BMI measurements, comorbidity status, and quality of life, assessed through the Bariatric Analysis and Reporting Outcome System (BAROS) questionnaire. Results: At one year postoperatively, the average excess body weight loss percentage (EBWL%) reached 64.43%, peaking at 79.31% at 18 months, with stabilization at 65.13% by the two-year mark. The average BMI decreased from 38.71 kg/m² preoperatively to 30.35 kg/m² at two years postoperatively. Obesity-related comorbidities showed significant improvement: 15 out of 16 patients with dyslipidemia and 10 out of 12 with hyperglycemia experienced resolution or improvement, while all 18 patients with joint pain reported symptom relief. Conclusions: LGCP has proven to be an effective bariatric procedure, delivering substantial weight loss and improving obesity-related conditions and QOL in patients with a BMI =35 kg/m². Despite these favorable outcomes, long-term success remains contingent on patient adherence to lifestyle modifications and postoperative guidelines.