Study type: In vivo/preclinical · Status: Evidence verified by machine against declared source

CerebrolysinTM efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure.

BMC neuroscience · 2014

Study scale: Error bars represent mean ± SEM (n = 6 per group, 6 m/o).

Product or molecular entity relationships

Cerebrolysin: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.

Public plain-language summary

The published text is limited to the declared source and preserves reported uncertainty. It does not establish efficacy, safety, suitability, or evidence strength.

Research question

For this purpose we sought to investigate the effects of CBL in a tg model of tauopathy.

Study design

We have previously shown that CerebrolysinTM (CBL), a neuropeptide mixture with neurotrophic effects, ameliorates the behavioral deficits and neuropathological alterations in amyloid precursor protein (APP) transgenic (tg) mouse model of AD by reducing hyper-phosphorylated Tau.

Participants or experimental system

Accordingly, double tg mice expressing mutant Tau under the mThy-1 promoter and GSK3β (to enhance Tau phosphorylation) were treated with CBL and evaluated neuropathologically.

Study scale

Error bars represent mean ± SEM (n = 6 per group, 6 m/o).

Intervention or exposure

CBL treatment reduced the levels of Tau phosphorylation in the dentate gyrus and the degeneration of pyramidal neurons in the temporal cortex and hippocampus of the Tau/GSK3β double tg mice.

Comparator

Compared to single Tau tg mice the Tau/GSK3β double tg model displayed elevated levels of Tau phosphorylation and neurodegeneration in the hippocampus.

Outcomes examined

Interestingly, the Tau/GSK3β double tg mice also displayed elevated levels of Dynamin-related protein-1 (Drp-1), a protein that hydrolyzes GTP and is required for mitochondrial division.

Key findings

These disorders are associated with Tau accumulation.

Limitations and uncertainty

Alzheimer’s Disease (AD) and Fronto temporal lobar dementia (FTLD) are common causes of dementia in the aging population for which limited therapeutical options are available.

Product relevance and evidence boundary

This record is a published study, held here with its citation and review status. It is not a statement that any catalog item is effective, safe, or suitable for any use, and nothing in it is a dose or a protocol.

Evidence verified by machine against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.