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AD

AD-220 (AD 220A / AD 220 / AD220)

✓ Approved

Addpharma · 小分子 · 小分子

什么是 AD-220？

AD-220 是一种小分子，由Addpharma研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名AD 220A, AD 220, AD220
公司Addpharma
药物类别小分子
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, Addpharma

治疗适应症

AD-220 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHyperlipidaemia✓ Approved
Metabolism and nutrition disordersHypercholesterolaemiaPreclinical

相关研究文献

PubMedFrontiers in neurology2026-09-11

Expression differences and diagnostic efficacy of core plasma biomarkers in Alzheimer's disease, cerebral small vessel disease and healthy adults.

Xiandong Wang W, Junqi Wu W, Xuan Zhang Z, Daichao Ma M et al.

Alzheimer's disease (AD) and cerebral small vessel disease (CSVD) are the two leading causes of cognitive impairment in the elderly, with overlapping clinical manifestations. This study aimed to explore the expression differences of plasma Aβ1-42, Aβ1-40, Aβ1-42/Aβ1-40, p-Tau181, p-Tau217, NfL and GFAP among patients with AD, CSVD and healthy populations, and to evaluate the diagnostic value of these biomarkers for AD as well as the differential diagnostic efficacy between AD and CSVD. A total of 120 participants were enrolled and divided into AD group, CSVD group and healthy control group, with 40 cases in each group. Plasma biomarkers were detected by chemiluminescence immunoassay, and cognitive function and neuroimaging examinations were completed simultaneously. The differences of biomarker levels among the three groups were compared. Spearman correlation analysis was used to analyze the correlation between each biomarker and MMSE score, and ROC curve was adopted to evaluate the diagnostic and differential diagnostic efficacy of single biomarker. Plasma Aβ1-42 and Aβ1-42/Aβ1-40 ratio were significantly decreased, while p-Tau181 and p-Tau217 were markedly elevated in the AD group. The GFAP level in the CSVD group was specifically and significantly higher than that in the AD group and healthy control group. NfL was significantly increased in both disease groups. p-Tau217 exhibited optimal efficacy in distinguishing AD from healthy controls (AUC = 0.894) and differentiating AD from CSVD (AUC = 0.877). GFAP showed excellent diagnostic value in distinguishing CSVD from healthy controls (AUC = 0.881). All biomarkers were significantly correlated with MMSE scores. Among patients with isolated AD or isolated CSVD, plasma p-Tau217 is the optimal specific biomarker for the diagnosis of AD and differentiation between AD and cerebral small vessel disease. GFAP acts as a key indicator for identifying CSVD. These findings should be interpreted cautiously for patients with AD-CSVD co-pathology. Combined detection of multiple plasma biomarkers provides an important clinical basis for non-invasive early screening and etiological classification of cognitive impairment in patients with pathologically isolated cognitive disorders.

PMID 42723835
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PubMedGenes, brain, and behavior2026-09-11

An Integrated Analysis of Manganese Metabolism-Related Genes and Their Association With Biomarkers, Immune Infiltration, and Clinical Subtypes in Alzheimer's Disease.

Shu Shengnan S, Hu Jiahao J, Hu Shanshan S, Yao Yefeng Y

Alzheimer's disease (AD), a neurodegenerative condition marked by amyloid-beta plaques and tau protein neurofibrillary tangles, progresses against a backdrop of essential biological processes. Manganese, an indispensable trace element for vital functions including energy metabolism and antioxidant defense, is integral to neurological health. Its precise metabolic role throughout the course of AD pathogenesis is not fully elucidated. Four essential manganese metabolism-related genes were identified as diagnostic markers through a multi-omic framework. This approach integrated Weighted Gene Co-Expression Network Analysis with machine learning ensembles (Least Absolute Shrinkage and Selection Operator/Random Forest/Extreme Gradient Boosting), followed by rigorous testing in an independent dataset. Beyond identification, we utilized CIBERSORT and ssGSEA to characterize immune infiltration and leveraged GSEA/GO/KEGG for pathway elucidation. Finally, AD patients were stratified into molecular subgroups based on these hub genes, and their underlying regulatory networks involving miRNAs and transcription factors were reconstructed. An integrated bioinformatics framework identified 12 differentially expressed genes related to manganese metabolism in AD. Machine-learning-based feature selection further pinpointed four key diagnostic biomarkers (TSPO, PTBP1, GLO1, and ACACB) with high discriminative power (AUC: 0.831-0.905). Immune infiltration analysis revealed substantial immune remodeling in AD, including an elevation of naïve B cells. Moreover, AD samples were classified into two molecular subtypes displaying distinct immune and metabolic characteristics, and regulatory miRNA/TF interaction networks were constructed for the core genes. Our results shed new light on the molecular mechanisms underlying AD and support future efforts toward early diagnosis and personalized therapeutic interventions based on molecular subtypes.

PMID 42723412
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PubMedAnnals of medicine and surgery (2012)2026-09-11

Microvascular damage in diabetic nephropathy and the subsequent risk of Alzheimer's disease: a systematic review.

Mohammed Noura N, Alyazan Khalil Taher Al-Jabali Tho T, Yassien Nuha N, Osman Abufatima Iman I et al.

Diabetic nephropathy (DN), a major microvascular complication of diabetes, is increasingly implicated in systemic vascular dysfunction and may contribute to the pathogenesis of Alzheimer's disease (AD). Microvascular injury is a recognized mechanism in AD, and DN-related damage may raise the risk of cognitive decline. Following the PRISMA 2020 guidelines, we searched PubMed, Scopus, and the Cochrane Library (2000-2025) for studies on DN-related vascular damage and cognitive outcomes. Quality was assessed using the Newcastle-Ottawa Scale and the AXIS tool. Of 275 records, nine studies were included (cross-sectional and longitudinal, with up to 37.5 years of follow-up). DN was measured via eGFR, albuminuria, the fibrinogen-to-albumin ratio, or ICD codes; cognition via assessed using amyloid PET, neurocognitive tests, or registry data. All studies found that impaired kidney function was associated with a greater risk of AD or cognitive decline. Available evidence links DN-related microvascular damage to a higher risk of AD, suggesting a kidney-brain axis. However, causality remains uncertain and requires longitudinal and mechanistic studies to clarify these pathways.

PMID 42724815
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PubMedJournal of thoracic disease2026-09-11

Association between serum anion gap and 28-day mortality among patients admitted to the hospital with aortic dissection: a retrospective cohort study with the MIMIC-IV database.

Chen Ke-Yuan KY, Lei Jian J, Yang Xi X, Zheng Ling-Zhao LZ et al.

The relationship between serum anion gap (AG) and mortality in aortic dissection (AD) patients remains unclear. This study aimed to elucidate the association between AG levels and 28-day mortality in patients with AD. This cohort study included AD patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Kaplan-Meier survival curves, Cox proportional hazards regression, and restricted cubic spline (RCS) were utilized to analyze the association between AG levels and 28-day mortality. Additionally, receiver operating characteristic (ROC) curves were employed to compare the predictive ability of AG and other serum ions for mortality. A total of 386 AD patients were included in the study. Multivariate analysis demonstrated that higher levels of AG were significantly associated with increased 28-day mortality [hazard ratio (HR) =1.43; 95% confidence interval (CI): 1.25-1.62; P<0.001]. Stratified analysis suggested that higher AG levels were associated with worse prognosis in older and female patients. RCS indicated a non-linear relationship between AG levels and 28-day mortality, with a turning point at 16.568 mEq/L. The ROC curves revealed that AG had a superior ability to predict 28-day mortality compared with other serum ions. Higher levels of AG were associated with increased 28-day mortality in AD patients, especially among elderly and female patients. AG demonstrated greater predictive ability for mortality compared with other serum ions.

PMID 42724524
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PubMedJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2026-09-11

EXPRESS: Rapamycin increases cerebral blood flow and modulates metabolic, inflammatory, and microbiome profiles in healthy middle-aged APOE4 carriers: a pilot single-arm trial.

Aware Chetan C, Neher Caitlin Maria CM, Woods Carter C, Khegai Oleksandr O et al.

Carriers of the apolipoprotein E4 (APOE4) allele often develop cerebrovascular dysfunction and broader systemic alterations decades before the onset of Alzheimer's disease (AD) pathology or clinical symptoms. Early interventions that can improve these functions may help delay or slow AD progression. In this study, we repurposed rapamycin (sirolimus), an FDA-approved medication with anti-aging properties, to target APOE4 associated multisystem dysfunction. We conducted a single arm trial of low dose rapamycin (1 mg/day for 4 weeks) in cognitively normal adults aged 45 to 65 years, prior to detectable AD pathology, stratified by APOE genotype. The primary outcome was cerebral blood flow (CBF), while secondary outcomes included plasma metabolomics, inflammatory cytokines, AD biomarkers, and gut microbiome composition. Twenty-three participants completed the study, including nine APOE4 carriers and fourteen non-carriers. Rapamycin significantly increased CBF in APOE4 carriers, with increases exceeding 15% across multiple brain regions, and improved metabolic and inflammatory profiles with minimal adverse effects. In contrast, non-carriers showed no significant change in CBF and exhibited distinct physiological responses, highlighting genotype dependent effects. These findings suggest that rapamycin may mitigate early cerebrovascular and systemic dysfunction in APOE4 carriers and support a precision medicine approach in which therapeutic response is influenced by genotype.

PMID 42723264
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PubMedClinical and experimental hepatology2026-09-11

Neutrophil-to-lymphocyte ratio in acute decompensation of advanced chronic liver disease and acute-on-chronic liver failure: prognostic significance by etiology.

Žilinčanová Daniela D, Adamcova Selcanova Svetlana S, Havaj Daniel J DJ, Šulejová Karolína K et al.

The neutrophil-to-lymphocyte ratio (NLR) is a simple and widely available indicator of the degree and balance of the systemic inflammatory response in critically ill patients and has been shown to predict outcomes across multiple liver syndromes, including alcohol-associated hepatitis, advanced chronic liver disease/liver cirrhosis (ACLD), and acute-on-chronic liver failure (ACLF). While NLR retains prognostic power throughout the spectrum of ACLD phenotypes, its performance may vary according to the underlying etiology of ACLD. Since efforts are ongoing to identify accessible inflammatory markers for risk stratification in ACLF, NLR has gained increasing attention. The primary aim was to determine whether NLR values differ between alcoholic, viral, and other etiologies of acute decompensation (AD), with particular focus on alcoholic liver disease (ALD). Secondary aims were to assess the prognostic potential of NLR measured at admission (NLR-0) and on day 7 of hospital stay (NLR-7). Using our RH7 registry of adult patients hospitalized with cirrhosis, we identified individuals with AD according to EF-CLIF criteria and stratified them into three etiological groups: alcoholic, viral, and "other". NLR-0 and NLR-7 values were compared across groups and related to 30-day, 90-day, and 1-year mortality. Out of 1109 patients in RH7 (as of May 18th, 2020), 283 were hospitalized for AD. Of these, 207 (73.1%) had ALD, 22 (7.8%) viral hepatitis, and 54 (19.1%) other causes of cirrhosis. The mean age was 51.3 years and 41% were women. Elevated NLR-0 and NLR-7 values were found in 219 (77.4%) and 138 (74.2%) patients, respectively. Elevated NLR-0 values were most frequent in ALD (80.2%), compared to 77.8% in other etiologies and only 50% in viral cases (p < 0.01). Both NLR-0 and NLR-7 were significantly lower in survivors vs. non-survivors across all etiologies (p < 0.01). No significant changes were observed between NLR-0 and NLR-7. In our Central European cohort, AD most frequently developed on the background of ALD, while viral etiology was rare. Elevated NLR was observed in the majority of patients admitted with AD and was consistently associated with increased short-, mid- and long-term mortality. Although NLR values were broadly comparable across etiologies, patients with viral AD had normal NLR significantly more often, suggesting possible differences in inflammatory phenotypes. These findings support the use of NLR as an additional prognostic marker, particularly in ALD, while highlighting the need for further studies in viral cohorts.

PMID 42724948
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