UMIN-CTR Clinical Trial
| Unique ID issued by UMIN | UMIN000024913 |
|---|---|
| Receipt number | R000028660 |
| Scientific Title | Analysis of Alzheimer disease mechanism using iPS derived human cortical neuron |
| Date of disclosure of the study information | 2016/11/21 |
| Last modified on | 2017/12/20 16:34:25 |
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Basic information
Public title
Analysis of Alzheimer disease mechanism using iPS derived human cortical neuron
Acronym
Analysis of Alzheimer disease mechanism using iPS derived human cortical neuron
Scientific Title
Analysis of Alzheimer disease mechanism using iPS derived human cortical neuron
Scientific Title:Acronym
Analysis of Alzheimer disease mechanism using iPS derived human cortical neuron
Region
| Japan |
Condition
Condition
Alzheimer's Disease
Classification by specialty
| Psychiatry |
Classification by malignancy
Others
Genomic information
NO
Objectives
Narrative objectives1
By using iPS-derived cortical neurons of AD and non AD control, we aim to analyze Abeta production mechanism and effects of disease course modifiers.
Basic objectives2
Pharmacokinetics
Basic objectives -Others
Trial characteristics_1
Exploratory
Trial characteristics_2
Explanatory
Developmental phase
Assessment
Primary outcomes
We aim to analyze Abeta production mechanism and effects of disease course modifiers.
Key secondary outcomes
Base
Study type
Observational
Study design
Basic design
Randomization
Randomization unit
Blinding
Control
Stratification
Dynamic allocation
Institution consideration
Blocking
Concealment
Intervention
No. of arms
Purpose of intervention
Type of intervention
Interventions/Control_1
Interventions/Control_2
Interventions/Control_3
Interventions/Control_4
Interventions/Control_5
Interventions/Control_6
Interventions/Control_7
Interventions/Control_8
Interventions/Control_9
Interventions/Control_10
Eligibility
Age-lower limit
| 60 | years-old | <= |
Age-upper limit
| 80 | years-old | > |
Gender
Male and Female
Key inclusion criteria
Alzheimer's disease patients and non-AD patients
Key exclusion criteria
other dementia than AD
Target sample size
8
Research contact person
Name of lead principal investigator
| 1st name | |
| Middle name | |
| Last name | Masayasu Okochi |
Organization
Osaka University Graduate School of Medicine
Division name
Department of Neuropsychiatry
Zip code
Address
D3 2-2 Yamadaoka Suita, Osaka Japan
TEL
+81-6879-3051
mokochi@psy.med.osaka-u.ac.jp
Public contact
Name of contact person
| 1st name | |
| Middle name | |
| Last name | Masayasu Okochi |
Organization
Osaka University Graduate School of Medicine
Division name
Department of Neuropsychiatry
Zip code
Address
D3 2-2 Yamadaoka Suita, Osaka Japan
TEL
+81-6879-3051
Homepage URL
mokochi@psy.med.osaka-u.ac.jp
Sponsor or person
Institute
Osaka University
Institute
Department
Personal name
Funding Source
Organization
Others
Organization
Division
Category of Funding Organization
Profit organization
Nationality of Funding Organization
Japan
Other related organizations
Co-sponsor
Shionogi pharmaceutical company
Name of secondary funder(s)
IRB Contact (For public release)
Organization
Address
Tel
Secondary IDs
Secondary IDs
NO
Study ID_1
Org. issuing International ID_1
Study ID_2
Org. issuing International ID_2
IND to MHLW
Institutions
Institutions
大阪大学大学院医学系研究科
Other administrative information
Date of disclosure of the study information
| 2016 | Year | 11 | Month | 21 | Day |
Related information
URL releasing protocol
Publication of results
Published
Result
URL related to results and publications
https://www.ncbi.nlm.nih.gov/pubmed/28978478
Number of participants that the trial has enrolled
Results
gamma-secretase inhibitors (GSI) are drugs developed to decrease amyloid-beta peptide (Abeta) production by inhibiting intramembranous cleavage of beta-amyloid protein precursor (betaAPP). However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with Alzheimer's disease (AD) was terminated due to unexpected aggravation of cognitive deficits and side effects. Here, we show that some semagacestat effects are clearly different from a phenotype caused by a loss of function of presenilins, core proteins in the gamma-secretase complex. Semagacestat increases intracellular byproduct peptides, produced along with Abeta through serial gamma-cleavage of betaAPP, as well as intracellular long Abeta species, in cell-based and in vivo studies of AD model mice. Other potential non-TSA GSIs, but not L685,458, a TSA GSI, have similar effects. Furthermore, semagacestat inhibits release of de novo intramembranous gamma-byproducts to the soluble space. Thus, semagacestat is a pseudo-GSI, and therefore, the semagacestat clinical trial did not truly test the Abeta hypothesis.
Results date posted
Results Delayed
Results Delay Reason
Date of the first journal publication of results
Baseline Characteristics
Participant flow
Adverse events
Outcome measures
Plan to share IPD
IPD sharing Plan description
Progress
Recruitment status
Completed
Date of protocol fixation
| 2015 | Year | 02 | Month | 02 | Day |
Date of IRB
Anticipated trial start date
| 2015 | Year | 02 | Month | 02 | Day |
Last follow-up date
Date of closure to data entry
Date trial data considered complete
Date analysis concluded
Other
Other related information
The results are described in the Results. Other studies using iPS derived neurons are on going.
Management information
Registered date
| 2016 | Year | 11 | Month | 19 | Day |
Last modified on
| 2017 | Year | 12 | Month | 20 | Day |
Link to view the page
Value
https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000028660
| Research Plan | |
|---|---|
| Registered date | File name |
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| Registered date | File name |
| Research case data | |
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| Registered date | File name |
