In this research the total mRNA-Tau expression is elevated in the cerebellum of mSOD1 mice the entire life span but the Tau protein is decrease at symptomatic stage. Because RNA binding proteins and RNA editing is implicated in ALS there may be a clue here that is relevant.

Amyloid protein found in Alzheimer's, Parkinson's, and Type II Diabetes was also reported to be implicated in ALS as well at the MNDA Conference in Sydney, AU 2012. Although amyloid and tau are different, they are connected in some way.

Any research that may explain the elusive yet relentless progession of neurodegeneration is important to include here on the Forum. ALS is not an elite disease that stands alone but a subtype of a large all encompassing group which is why ALS research is found on the Alzheimer's Forum. As an orphan disease it is important that the ALSTDI Forum have a policy and spirit of collaboration with research of other nuerodegenerative diseases.

Kind regards,

Donnna

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Neurochem Res. 2007 Mar;32(3):415-21.

Age-related changes in tau expression in transgenic mouse model of amyotrophic lateral sclerosis.

Barańczyk-Kuźma A, Usarek E, Kuźma-Kozakiewcz M, Kaźmierczak B, Gajewska B, Schwalenstocker B, Ludolph AC.

Department of Biochemistry, Medical University of Warsaw, Banacha 1, Warsaw 02-097, Poland

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.