ArticleNeurochemical research2007
Age-related changes in tau expression in transgenic mouse model of amyotrophic lateral sclerosis.
Article in Neurochemical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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, 11 citations in OpenAlex.
- Cerebellum in Alzheimer's disease and other neurodegenerative diseases: an emerging research frontier.MedComm · 2024Review
- Cerebellar pathology in motor neuron disease: neuroplasticity and neurodegeneration.Neural regeneration research · 2022Review
- Could Sirtuin Activities Modify ALS Onset and Progression?Cellular and molecular neurobiology · 2017Review
- Overexpression of Human SOD1 Leads to Discrete Defects in the Cerebellar Architecture in the Mouse.Frontiers in neuroanatomy · 2017Article
- Mice with mutation in dynein heavy chain 1 do not share the same tau expression pattern with mice with SOD1-related motor neuron disease.Neurochemical research · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The work is a continuation of studies on tau expression and alternative splicing in the central nervous system of transgenic mice harboring human SOD1 with G93A amyotrophic lateral sclerosis (ALS)-associated mutation. Since age is an important risk factor for ALS, we expanded the studies into younger animals (age 5 and 25 days). We also included cerebellum, a structure not studied in the context of neurodegeneration in ALS. We found decreased total tau-mRNA expression in hippocampus but not in cortex and spinal cord of young transgenics, and a lack of exon 10 in 5-day-old mice. In cerebellum, the total tau-mRNA expression was increased in transgenic animals during the whole period of life, however at the symptomatic stage of ALS (age 120 days) the level of protein was decreased. It can be concluded that the SOD1 G93A mutation causes early alterations of tau expression in cns, which are not exclusively restricted to the upper and lower motor neuron.
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Registered trials
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