ArticleJournal of neuropathology and experimental neurology2010
Genetic ablation of luteinizing hormone receptor improves the amyloid pathology in a mouse model of Alzheimer disease.
Article in Journal of neuropathology and experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 44 citations in OpenAlex.
- Gonadotropins Across the Lifespan: Their role in the Neurodevelopment-Neurodegeneration Continuum.The Yale journal of biology and medicine · 2026Review
- Long-term systemic androgen deprivation partially modulates neuroinflammation in male AppScientific reports · 2025Article
- Endocrine Dyscrasia in the Etiology and Therapy of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Review
- Mechanisms linking neurological disorders with reproductive endocrine dysfunction: Insights from epilepsy research.Frontiers in neuroendocrinology · 2023Review
- Effect of exercise on the hypothalamic-pituitary-gonadal axis in a rat model of Alzheimer's disease.Scientific reports · 2023Article
- Alternative Pharmacological Strategies for the Treatment of Alzheimer's Disease: Focus on Neuromodulator Function.Biomedicines · 2022Review
- Article
- Rationale, study design and implementation of the LUCINDA Trial: Leuprolide plus Cholinesterase Inhibition to reduce Neurologic Decline in Alzheimer's.Contemporary clinical trials · 2021Article
- Glycoprotein G-protein Coupled Receptors in Disease: Luteinizing Hormone Receptors and Follicle Stimulating Hormone Receptors.Diseases (Basel, Switzerland) · 2020Review
- Possible Existence of the Hypothalamic-Pituitary-Hippocampal (HPH) Axis: A Reciprocal Relationship Between Hippocampal Specific Neuroestradiol Synthesis and Neuroblastosis in Ageing Brains with Special Reference to Menopause and Neurocognitive Disorders.Neurochemical research · 2019Review
- Human chorionic gonadotropin attenuates amyloid-β plaques induced by streptozotocin in the rat brain by affecting cytochrome c-ir neuron density.Iranian journal of basic medical sciences · 2019Article
- Molecular and functional insights into gonadotropin hormone receptor dimerization and oligomerization.Minerva ginecologica · 2018Review
- Luteinizing Hormone Involvement in Aging Female Cognition: Not All Is Estrogen Loss.Frontiers in endocrinology · 2018Review
- Non-conventional expression systems for the production of vaccine proteins and immunotherapeutic molecules.Human vaccines & immunotherapeutics · 2017Review
- Metabolic and Non-Cognitive Manifestations of Alzheimer's Disease: The Hypothalamus as Both Culprit and Target of Pathology.Cell metabolism · 2015Review
- The endocrine dyscrasia that accompanies menopause and andropause induces aberrant cell cycle signaling that triggers re-entry of post-mitotic neurons into the cell cycle, neurodysfunction, neurodegeneration and cognitive disease.Hormones and behavior · 2015Review
- A Unified Hypothesis of Early- and Late-Onset Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2015Review
- Sex and gonadal hormones in mouse models of Alzheimer's disease: what is relevant to the human condition?Biology of sex differences · 2012Article
- Evaluation of the effects of testosterone and luteinizing hormone on regulation of β-amyloid in male 3xTg-AD mice.Brain research · 2012Article
- Animal models for aberrations of gonadotropin action.Reviews in endocrine & metabolic disorders · 2011Review
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 at 3 institutions in 2 countries.
Funding
Abstract
Amyloid-beta peptide (Abeta) plays an essential pathophysiologic role in Alzheimer disease, and elevation of luteinizing hormone (LH) levels during aging has been implicated in its pathogenesis. To assess the effect of LH receptor deficiency on Abeta accumulation, we generated a bigenic mouse model, APPsw(+)/Lhr(-/-), which expresses human amyloid precursor protein (APPsw) in the background of LH receptor (Lhr) knockout. Genetic ablation of Lhr resulted in a significant decrease in the number of Abeta plaques and protein content in the hippocampus and cerebral cortex in both male and female mice. Accordingly, several Abeta deposition-related neuropathologic features and functionally relevant molecules were markedly improved, including decreased astrogliosis, reductions of elevated phosphorylated tau, c-fos, alpha7-nicotinic acetylcholine receptor, and restoration of the altered neuropeptide Y receptors Y1 and Y2. Diminution of Abeta accumulation in the absence of LH receptor supports the contention that dysregulation of LH may impact the pathogenesis of Alzheimer disease. The APPsw(+)/Lhr(-/-) mouse may be a useful tool for advancing understanding of the role of LH-mediated events in Alzheimer disease and a model in which to test therapeutic interventions.
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.