Alzheimer’s disease (AD), a primary neurodegenerative disorder, is characterized by amyloid-β plaques and tau hyperphosphorylation-induced neurofibrillary tangles. Current treatments only alleviate symptoms, and Aβ monoclonal antibodies raise safety concerns in clinical use. Natural components (NCs) of Traditional Chinese Medicine (TCM) (eg, curcumin, quercetin, berberine, resveratrol) exhibit multi-target neuroprotective effects in AD, but poor blood-brain barrier (BBB) penetration and low bioavailability limit clinical use. Recent strategies to enhance TCM delivery include NP-based nanoparticle (NP) drug delivery systems (NDDS), structural modifications, and combination therapies. NDDS demonstrate superior performance in enabling brain-targeting delivery via passive (paracellular/transcellular) and active (adsorption-/receptor-/carrier-mediated transcytosis) approaches, improving NCs’ stability, controlled release, and bioavailability. With NCs of TCM delivery via NDDS, it is possible to develop intelligent therapeutic systems that combine multi-target regulation with precise drug delivery. This review summarizes the diverse neuroprotective effects of NCs of TCM in AD treatment and discusses the commonly used types of NPs for AD therapy. It particularly focuses on these NCs of TCM delivery via NDDS, covering aspects such as NPs types, fabrication techniques, characteristics, administration routes, and advantages. Finally, the challenges and potential solutions for NCs of TCM were examined, along with comparative advantages and limitations among different NPs and future research directions. Collectively, NCs of TCM delivery via NDDS demonstrate promising therapeutic potential for AD treatment.

The major pathological feature of Alzheimer’s disease (AD) is the aggregation of amyloid β peptide (Aβ) in the brain. Inhibition of Aβ₄₂ aggregation may prevent the advancement of AD. This study employed molecular dynamics, molecular docking, electron microscopy, circular dichroism, staining of aggregated Aβ with ThT, cell viability, and flow cytometry for the detection of reactive oxygen species (ROS) and apoptosis. Aβ₄₂ polymerizes into fibrils due to hydrophobic interactions to minimize free energy, adopting a β-strand structure and forming three hydrophobic areas. Eight dipeptides were screened by molecular docking from a structural database of 20 L-α-amino acids, and the docking was validated by molecular dynamics (MD) analysis of binding stability and interaction potential energy. Among the dipeptides, arginine dipeptide (RR) inhibited Aβ₄₂ aggregation the most. The ThT assay and EM revealed that RR reduced Aβ₄₂ aggregation, whereas the circular dichroism spectroscopy analysis showed a 62.8% decrease in β-sheet conformation and a 39.3% increase in random coiling of Aβ₄₂ in the presence of RR. RR also significantly reduced the toxicity of Aβ₄₂ secreted by SH-SY5Y cells, including cell death, ROS production, and apoptosis. The formation of three hydrophobic regions and polymerization of Aβ₄₂ reduced the Gibbs free energy, and RR was the most effective dipeptide at interfering with polymerization.

Background: Baseline sarcopenia has been linked to cognitive decline in older adults; however, the impact of longitudinal changes in sarcopenia status on cognitive trajectories remains unclear. Objective: This aims to examine the association between 2-year transitions in sarcopenia status and subsequent 5-year cognitive trajectories among middle-aged and older adults in China. Methods: We analyzed data from 8189 participants (median age 58, IQR y; n=432952.9% female) in the China Health and Retirement Longitudinal Study. Sarcopenia status was determined in 2011 and 2013 according to the 2019 Asian Working Group for Sarcopenia criteria, and participants were classified into 7 transition groups based on status changes. Cognitive function was assessed from 2013 to 2018 using standardized z scores for executive function and episodic memory. Linear mixed-effects models were applied to evaluate associations between sarcopenia transitions and cognitive trajectories, adjusting for demographic, lifestyle, and health-related covariates. Results: Progression from a nonsarcopenic state was associated with greater cognitive decline compared to stable nonsarcopenia ( β =–0.016, 95% CI –0.026 to –0.007; P <.001), with greater decline observed among those progressing from possible sarcopenia to sarcopenia ( β =–0.027, 95% CI –0.054 to –0.001; P =.04). In contrast, regression from possible sarcopenia was associated with improved cognitive performance ( β =0.028, 95% CI 0.015-0.041; P <.001). No significant improvement was observed among individuals regressing from established sarcopenia. Subgroup analyses showed consistent benefits of regression from possible sarcopenia across sex, age, residence, and education groups, except among urban residents ( P =.05). Conclusions: Progression in sarcopenia status was independently associated with accelerated cognitive decline, whereas regression from possible sarcopenia predicted cognitive benefit. These findings highlight possible sarcopenia as a clinically actionable and potentially reversible stage and underscore the importance of early identification and intervention to preserve cognitive health in aging populations.

Background Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune disease of the central nervous system (CNS) that often causes a range of neuropsychiatric symptoms; but with a relatively low recurrence rate. Anti-NMDAR encephalitis may occur with anti-myelin oligodendrocyte glycoprotein (MOG) encephalitis simultaneously or followed by anti-MOG encephalitis after several months. Case presentation We presented a case of recurrent anti-NMDAR encephalitis followed by anti-MOG encephalitis. A 39-year-old man was admitted to the hospital with five episodes of convulsive seizures, psychoses and memory deficits. With a positive Anti-NMDAR antibody in the cerebrospinal fluid (CSF), after being treated with intravenous immunoglobulins (IVIG) 22.5 g/day for 7 days, intravenous methylprednisolone pulse (IVMP) 500 mg/day for 4 days, and followed by IVMP 250 mg/day for 3 days, the patient was recovered completely. After 1 month, the patient developed disturbances of consciousness, speech difficulties and convulsions. With the positive result of Anti-NMDAR antibodies in the CSF again, we confirmed the diagnosis of recurrent anti-NMDAR encephalitis. The patient was then fully recovered after treatment with IVIG, IVMP and rituximab. Six months later, the patient was readmitted to the hospital with occasional convulsions. With a positive serum MOG antibody and a lesion in the right brainstem by brain magnetic resonance imaging (MRI), the patient was confirmed for anti-MOG encephalitis. The patient was fully recovered again after treatment with IVMP and rituximab, with no neurological sequels remained. Conclusion Patients with positive MOG antibodies are more likely to have brainstem MRI lesions than those with anti-NMDAR encephalitis. Rituximab is recommended for recurrent anti-NMDAR and anti-MOG encephalitis.