Evidence map›Paper›PMID 25514752›Full record

ArticleTranslational psychiatry2014

Identification of tetrahydrocarbazoles as novel multifactorial drug candidates for treatment of Alzheimer's disease.

K Honarnejad, A Daschner, A P Gehring, A Szybinska, A Giese, J Kuznicki, F Bracher, J Herms

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

K Honarnejad1] Department of Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany [2] Center for Neuropathology and Prion Research, Ludwig Maximilian University, Munich, Germany [3] Graduate School of Systemic Neurosciences, Ludwig Maximilian University, Munich, Germany.
A Daschner1] Department of Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany [2] Center for Neuropathology and Prion Research, Ludwig Maximilian University, Munich, Germany.
A P GehringDepartment of Pharmacy, Center for Drug Research, Ludwig Maximilian University, Munich, Germany.
A SzybinskaLaboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland.
A GieseCenter for Neuropathology and Prion Research, Ludwig Maximilian University, Munich, Germany.
J KuznickiLaboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland.
F BracherDepartment of Pharmacy, Center for Drug Research, Ludwig Maximilian University, Munich, Germany.
J Herms1] Department of Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany [2] Center for Neuropathology and Prion Research, Ludwig Maximilian University, Munich, Germany [3] Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
Ludwig-Maximilians-Universität München · DEGerman Center for Neurodegenerative Diseases · DEInternational Institute of Molecular and Cell Biology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative brain disorder and the most frequent cause of dementia. To date, there are only a few approved drugs for AD, which show little or no effect on disease progression. Impaired intracellular calcium homeostasis is believed to occur early in the cascade of events leading to AD. Here, we examined the possibility of normalizing the disrupted calcium homeostasis in the endoplasmic reticulum (ER) store as an innovative approach for AD drug discovery. High-throughput screening of a small-molecule compound library led to the identification of tetrahydrocarbazoles, a novel multifactorial class of compounds that can normalize the impaired ER calcium homeostasis. We found that the tetrahydrocarbazole lead structure, first, dampens the enhanced calcium release from ER in HEK293 cells expressing familial Alzheimer's disease (FAD)-linked presenilin 1 mutations. Second, the lead structure also improves mitochondrial function, measured by increased mitochondrial membrane potential. Third, the same lead structure also attenuates the production of amyloid-beta (Aβ) peptides by decreasing the cleavage of amyloid precursor protein (APP) by β-secretase, without notably affecting α- and γ-secretase cleavage activities. Considering the beneficial effects of tetrahydrocarbazoles addressing three key pathological aspects of AD, these compounds hold promise for the development of potentially effective AD drug candidates.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCalciumCarbazolesDrug DiscoveryEndoplasmic ReticulumHEK293 CellsHomeostasisHumansMitochondriaAmyloid beta-PeptidesCalciumCarbazoles

Identifiers

PMID25514752
PMCPMC4270312
OpenAlexW1965873851

What OpenQuestion holds

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Registered trials

None linked

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.