Early-onset Alzheimer's Disease Phenotypes: Neuropsychology and Neural Networks (EOAD-Subtype)
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT03153371|
Recruitment Status : Recruiting
First Posted : May 15, 2017
Last Update Posted : April 28, 2020
|Condition or disease|
|Alzheimer Disease, Early Onset Alzheimer Disease Alzheimer Disease, Late Onset Dementia, Alzheimer Type Logopenic Progressive Aphasia Primary Progressive Aphasia Visuospatial/Perceptual Abilities Posterior Cortical Atrophy Executive Dysfunction Corticobasal Degeneration Ideomotor Apraxia|
Unlike the usual late-onset Alzheimer's disease (LOAD), early-onset AD (EOAD), with onset before age 65, includes a high percentage of phenotypic variants. These non-familial, variants (vEOAD) present, not with progressive memory loss, but with language, visuospatial, or other cognitive difficulties. AD is now understood as a disorder that manifests with disturbed cognition reflecting disturbed neural networks. A multivariate analysis of neuropsychological tests, the "gold standard" for objectively defining neurocognitive impairments, coupled with structural and functional neuroimaging analysis of connectomes, can identify the neurocognitive-neural network profiles of vEOAD patients, compared to those with typical AD. This knowledge can increase our understanding of the heterogeneity of AD and how it causes disease.
This study hopes to show that vEOAD constitutes a "Type 2 AD", by (1) defining the neuropsychological components of Type 2 AD, and (2) understanding the anatomy and atrophy of the brains of vEOAD patients. Together, these components can outline the neurocognitive-neural network profile of Type 2 AD.
In addition to information that can help in the diagnosis and management of EOAD, this study can stimulate novel research into the reasons for this neurobiological heterogeneity in AD and could potentially lead to interventions based on alternate neurocognitive-neural network profiles.
|Study Type :||Observational|
|Estimated Enrollment :||180 participants|
|Official Title:||Early-onset Alzheimer's Disease Phenotypes: Neuropsychology and Neural Networks|
|Actual Study Start Date :||April 4, 2016|
|Estimated Primary Completion Date :||March 31, 2021|
|Estimated Study Completion Date :||March 31, 2022|
Early-onset Alzheimer's disease
This group will include 90 patients who have been diagnosed with clinically probable early-onset Alzheimer's disease by the UCLA Neurology Clinic (60 variant phenotypes; 30 typical amnestic).
This group will include 30 patients who have been diagnosed with clinically probable Alzheimer's disease (typical late-onset AD)
Healthy age-matched individuals without clinically significant cognitive impairments will be enrolled into this study.
- Alzheimer's disease Subtype [ Time Frame: Performed at baseline ]Neuropsychological testing results for use in a two-stage multivariate diagnostic method that combines the (weighted) test results in order to best discriminate Type 2 AD and typical AD.
- Change in overall Neurological profile [ Time Frame: Performed at baseline and 1-year follow-up visit ]Change in performance on neurological tasks between baseline visit and follow-up visit.
- Brain atrophy in MRI - Magnetic Resonance Imaging of the brain [ Time Frame: Performed at baseline visit ]Images from initial MRI scan taken at baseline visit will be analyzed for atrophy and white matter tract integrity
- Change in overall Neuropsychological profile [ Time Frame: Performed at baseline and 1-year follow-up visit ]Change in neuropsychological performance over time.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03153371
|Contact: Youssef I Khattab, BA||(310)-478-3711 ext 48176||YKhattab@mednet.ucla.edu|
|Contact: Elivra E Jimenez, PhD||(310)-478-3711 ext 40584 or email@example.com|
|United States, California|
|UCLA Department of Neurology||Recruiting|
|Los Angeles, California, United States, 90095|
|Contact: Youssef I Khattab, BA 310-478-3711 ext 48176 YKhattab@mednet.ucla.edu|
|Contact: Elvira E Jimenez, PhD (310)-478-3711 ext 40584 or 43389 firstname.lastname@example.org|
|Principal Investigator: Mario F Mendez, MD, PhD|
|Principal Investigator:||Mario F Mendez, MD, PhD||University of California, Los Angeles|