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Name:
UMIN ID:

Recruitment status Completed
Unique ID issued by UMIN UMIN000024913
Receipt No. 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

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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
Email 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
Email mokochi@psy.med.osaka-u.ac.jp

Sponsor
Institute Osaka University
Institute
Department

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
Email

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
URL(English) https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000028660

Research Plan
Registered date File name

Research case data specifications
Registered date File name

Research case data
Registered date File name


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