On 2015 Oct 03, Friedrich Thinnes commented:

miR-29 and VDAC-1

According to a recent paper of Reema Roshane et al. (2014) the expression of miR-29a is reduced in patients and animal models of several neurodegenerative disorders, including Alzheimer’s disease, Huntington’s disease, and spinocerebellar ataxias. Furthermore, the authors reported on cellular and behavioral effects of in vivo, brain-specific knockdown of miR-29. Large regions of the hippocampus and cerebellum showed massive cell death, reiterating the role of miR-29 in neuronal survival.

Interestingly, the apoptotic targets of miR-29, such as Puma, Bim, Bak, or Bace1, failed to show expected levels of up-regulation in mice, following knockdown of miR-29 while another miR-29 target, voltage dependent anion channel (VDAC-1), was found to be induced several fold in the hippocampus, cerebellum, and cortex of mice following miRNA knockdown.

Partial restoration of apoptosis was achieved by down-regulation of VDAC1 in miR-29 knockdown cells.

Anyway, it may pay to keep this observation on the schedule.

References

Roshan R, Shridhar S, Sarangdhar MA, Banik A, Chawla M, Garg M, Singh VP, Pillai B. (2014) Brain-specific knockdown of miR-29 results in neuronal cell death and ataxia in mice. RNA. 20:1287-1297. doi: 10.1261/rna.044008.113. Epub 2014 Jun 23. PMID: 24958907 Free PMC Article

Thinnes FP (2015) Plasmalemmal VDAC-1 corroborated as amyloid Aß-receptor. Front. Aging Neurosci., 30 September 2015 | http://dx.doi.org/10.3389/fnagi.2015.00188 OPINION ARTICLE

On 2015 Oct 03, Friedrich Thinnes commented:

miR-29 and VDAC-1

According to a recent paper of Reema Roshane et al. (2014) the expression of miR-29a is reduced in patients and animal models of several neurodegenerative disorders, including Alzheimer’s disease, Huntington’s disease, and spinocerebellar ataxias. Furthermore, the authors reported on cellular and behavioral effects of in vivo, brain-specific knockdown of miR-29. Large regions of the hippocampus and cerebellum showed massive cell death, reiterating the role of miR-29 in neuronal survival.

Interestingly, the apoptotic targets of miR-29, such as Puma, Bim, Bak, or Bace1, failed to show expected levels of up-regulation in mice, following knockdown of miR-29 while another miR-29 target, voltage dependent anion channel (VDAC-1), was found to be induced several fold in the hippocampus, cerebellum, and cortex of mice following miRNA knockdown.

Partial restoration of apoptosis was achieved by down-regulation of VDAC1 in miR-29 knockdown cells.

Anyway, it may pay to keep this observation on the schedule.

References

Roshan R, Shridhar S, Sarangdhar MA, Banik A, Chawla M, Garg M, Singh VP, Pillai B. (2014) Brain-specific knockdown of miR-29 results in neuronal cell death and ataxia in mice. RNA. 20:1287-1297. doi: 10.1261/rna.044008.113. Epub 2014 Jun 23. PMID: 24958907 Free PMC Article

Thinnes FP (2015) Plasmalemmal VDAC-1 corroborated as amyloid Aß-receptor. Front. Aging Neurosci., 30 September 2015 | http://dx.doi.org/10.3389/fnagi.2015.00188 OPINION ARTICLE