ArticleAlcohol (Fayetteville, N.Y.)2025
Alcohol consumption during early adulthood increases the vulnerability of locus coeruleus neurons and amyloid beta pathology in female APP/PS1 mice.
Article in Alcohol (Fayetteville, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Alcohol use disorder is the most common substance misuse disorder and Alzheimer's disease (AD) is the most common neurodegenerative disease. Evidence suggests that alcohol consumption may increase the risk for developing dementia and AD. The locus coeruleus (LC) is a region wherein the impact of alcohol and AD may converge. The LC is a noradrenergic nucleus that is highly vulnerable to degeneration in AD, and loss of LC neurons is associated with increased amyloid beta (Abeta) pathology. The present study examined whether alcohol consumption during early adulthood impacts LC degeneration and Abeta using the APP/PS1 mouse model. Female APP/PS1 mice underwent an eight-week chronic intermittent access (IA) alcohol consumption paradigm followed by twenty-three weeks of abstinence; water-consuming control subjects were run in parallel. APP/PS1 mice that had IA to alcohol showed a 21.9% decrease in the number of LC neurons and a decrease in the length of noradrenergic axons innervating the primary motor cortex. Furthermore, this alcohol induced LC deficit was associated with an increase in Abeta pathology in the primary motor cortex. In contrast to results from female APP/PS1 mice, there were no deficits in axon length and only a 9.4% decrease in the number of LC neurons in non-transgenic female subjects after abstinence from IA to alcohol. Our results demonstrate that alcohol consumption during early adulthood increases the vulnerability of LC neurons to degeneration and exacerbates Abeta pathology in female APP/PS1 mice, providing evidence that a history of alcohol abuse may impact the trajectory and severity of AD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.