Biology subjects

Barnett, A. G.

Publications and source records attributed to Barnett, A. G..

3 recordsLinked to original sources

bioRxiv2026

Suspected distortion of citations in high-impact cancer journals

Research and scholarship are shaped by article citations, which underpin the communication of ideas, assignment of credit, journal impact factors, and author career progression. Given their key influence on author and journal metrics, citations can be intentionally manipulated to inflate the reputation of journals and researchers. Paper mills, unethical organisations that produce and sell manuscripts and publishing services, may also be manipulating citations, but the extent of this manipulation is unknown. Here, we show that molecular cancer articles sharing features with retracted papers from paper mills display citation patterns that suggest systematic inflation. These articles were published in journals in the top decile of journal rankings. Suspected paper mill articles received 50 to 100% more citations than other papers 1 to 3 years after publication, while paradoxically attracting fewer readers and online accesses. Suspected paper mill articles also cited - and were cited by - other suspected paper mill articles, which frequently appeared in journals previously reported as paper mill targets. Citations from suspected paper mill articles measurably inflated journal citation metrics. These findings suggest that paper mills inflate the citation metrics of supported publications and affected journals at scale. This widespread manipulation of citation metrics may amplify unreliable findings, slowing scientific progress and spurring unreasonable citation benchmarks for research articles, journals and authors. Our findings point to measurable signatures of citation manipulation that could support article- and journal-level screening.

cancer biology↗

bioRxiv2025

Revealing the Paper Mill Iceberg: AI-Based Screening of Cancer Research Publications.

ObjectivesTo train and validate a machine learning model to distinguish paper mill publications from genuine cancer research articles, and to screen the cancer research literature to assess the prevalence of papers that have textual similarities to paper mill papers. DesignMethodological study applying a BERT-based text classification model to article titles and abstracts. SettingRetracted paper mill publications listed in the Retraction Watch database were used for model training. The cancer research corpus was screened by the model, using the PubMed database restricted to original cancer research articles published between 1999 and 2024. ParticipantsThe model was trained on 2,202 retracted paper mill papers and validated on independent data collected by image integrity experts. A total of 2.6 million cancer research papers were screened. Main outcome measuresClassification performance of the model. Prevalence of papers flagged as similar to retracted paper mill publications with 95% confidence intervals and their distribution over time, by country, publisher, cancer type, research area, and within high-impact journals (Decile 1). ResultsThe model achieved an accuracy of 0.91. When applied to the cancer research literature, it flagged 9.87% (95% CI 9.83 to 9.90) of papers and revealed a large increase in flagged papers from 1999 to 2024, both across the entire corpus and in the top 10% of journals by impact factor. Over 170,000 papers affiliated with Chinese institutions were flagged, accounting for 35% of Chinese cancer research articles. Most publishers had published substantial numbers of flagged papers. Flagged papers were overrepresented in fundamental research and in gastric, bone, and liver cancer. ConclusionsPaper mills are a large and growing problem in the cancer literature and are not restricted to low impact journals. Collective awareness and action will be crucial to address the problem of paper mill publications.

cancer biology↗

bioRxiv2024

Loss of neuronal lysosomal acid lipase drives amyloid pathology in Alzheimer's disease

Underlying drivers of late-onset Alzheimers disease (LOAD) pathology remain unknown. However, multiple biologically diverse risk factors share a common pathological progression. To identify convergent molecular abnormalities that drive LOAD pathogenesis we compared two common midlife risk factors for LOAD, heavy alcohol use and obesity. This revealed that disrupted lipophagy is an underlying cause of LOAD pathogenesis. Both exposures reduced lysosomal flux, with a loss of neuronal lysosomal acid lipase (LAL). This resulted in neuronal lysosomal lipid (NLL) accumulation, which opposed A{beta} localization to lysosomes. Neuronal LAL loss both preceded (with aging) and promoted (targeted knockdown) A{beta} pathology and cognitive deficits in AD mice. The addition of recombinant LAL ex vivo and neuronal LAL overexpression in vivo prevented amyloid increases and improved cognition. In WT mice, neuronal LAL declined with aging and correlated negatively with entorhinal A{beta}. In healthy human brain, LAL also declined with age, suggesting this contributes to the age-related vulnerability for AD. In human LOAD LAL was further reduced, correlated negatively with A{beta}1-42, and occurred with polymerase pausing at the LAL gene. Together, this finds that the loss of neuronal LAL promotes NLL accumulation to impede degradation of A{beta} in neuronal lysosomes to drive AD amyloid pathology. SummaryCellular and molecular drivers of late-onset Alzheimers disease (LOAD) are unknown, though several risk factors account for the majority of disease incidence1-5. Though diverse in their biological natures, each of these risk exposures converge on a shared pathological progression with the accumulation of amyloid early in the disease. Human genetic and transcriptomic studies suggest a role for altered lipid metabolism6-9, though the mechanism has been unknown. Here, using two common midlife risk exposures for LOAD, we found that dysfunctional lipophagy caused by the loss of lysosomal acid lipase (LAL) promotes early LOAD pathogenesis. Both midlife obesity and heavy alcohol reduced neuronal LAL, causing an increase in neuronal lysosomal lipid, and a subsequent accumulation of A{beta} in the extra-lysosomal cytosol. This loss of LAL preceded and promoted A{beta} pathology and cognitive deficits in AD mice. The addition of recombinant LAL ex vivo and neuronal LAL overexpression in vivo prevented increases in amyloid and improved cognition. In human brain, LAL declined with age in healthy subjects, similar to rodents, showing robust losses in LOAD subjects with polymerase pausing. Together, this implicates neuronal LAL loss in LOAD pathogenesis and presents LAL as a promising diagnostic, preventative, and/or therapeutic target for AD.

neuroscience↗