ArticleBiomedicines2022
Differential Neuropathology, Genetics, and Transcriptomics in Two Kindred Cases with Alzheimer's Disease and Lewy Body Dementia.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Genome-wide association study provides insights into the genetic basis of Lewy body dementia.Molecular psychiatry · 2025Pooled it
- Feeding All-Trans Retinoic Acid to Pregnant Sows Regulates the Development of the Pulmonary Nervous Systems of Neonatal Pigs.Veterinary sciences · 2026Article
- microRNA Expression in the Late Embryonic Pax6-Null Mouse Cerebellum.Molecular neurobiology · 2025Article
- Identification of Potentially Repurposable Drugs for Lewy Body Dementia Using a Network-Based Approach.Journal of molecular neuroscience : MN · 2024Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) and Lewy body dementia (LBD) are two different forms of dementia, but their pathology may involve the same cortical areas with overlapping cognitive manifestations. Nonetheless, the clinical phenotype is different due to the topography of the lesions driven by the different underlying molecular processes that arise apart from genetics, causing diverse neurodegeneration. Here, we define the commonalities and differences in the pathological processes of dementia in two kindred cases, a mother and a son, who developed classical AD and an aggressive form of AD/LBD, respectively, through a neuropathological, genetic (next-generation sequencing), and transcriptomic (RNA-seq) comparison of four different brain areas. A genetic analysis did not reveal any pathogenic variants in the principal AD/LBD-causative genes. RNA sequencing highlighted high transcriptional dysregulation within the substantia nigra in the AD/LBD case, while the AD case showed lower transcriptional dysregulation, with the parietal lobe being the most involved brain area. The hippocampus (the most degenerated area) and basal ganglia (lacking specific lesions) expressed the lowest level of dysregulation. Our data suggest that there is a link between transcriptional dysregulation and the amount of tissue damage accumulated across time, assessed through neuropathology. Moreover, we highlight that the molecular bases of AD and LBD follow very different pathways, which underlie their neuropathological signatures. Indeed, the transcriptome profiling through RNA sequencing may be an important tool in flanking the neuropathological analysis for a deeper understanding of AD and LBD pathogenesis.
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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.