Dominantly Inherited Alzheimer Network Trial: An Opportunity to Prevent Dementia. A Study of Potential Disease Modifying Treatments in Individuals With a Type of Early Onset Alzheimer's Disease Caused by a Genetic Mutation (DIAN-TU) (DIAN-TU)

• ClinicalTrials.gov Identifier: NCT05269394
• Recruitment Status: Recruiting
• First Posted: March 8, 2022
• Last Update Posted: February 22, 2024
• Sponsor: Washington University School of Medicine
• Collaborators: Alzheimer's Association; National Institute on Aging (NIA); Accelerating Medicines Partnership (AMP); Eisai Inc.
• Information provided by (Responsible Party): Washington University School of Medicine

Study Description

Brief Summary:

To assess the safety, tolerability, biomarker, cognitive, and clinical efficacy of investigational products in participants with an Alzheimer's disease-causing mutation by determining if treatment with the study drug improves disease-related biomarkers and slows the rate of progression of cognitive or clinical impairment.

Condition or disease	Intervention/treatment	Phase
Alzheimers Disease; Dementia; Alzheimers Disease, Familial	Drug: E2814; Drug: Lecanemab; Drug: Matching Placebo (E2814)	Phase 2; Phase 3

Detailed Description:

Alzheimer's disease (AD) is characterized pathologically by the presence of accumulation of amyloid plaques and tau-containing neurofibrillary tangles (NFTs) in the brain. Amyloid plaques can be detectable within the brain some years before symptoms manifest whereas tau-mediated toxicity has been hypothesized to appear later during the course of disease. Physiologically, tau is predominantly a neuronal microtubule-associated protein that plays a fundamental role in the stabilization of microtubules. Under pathological conditions however, short motifs in the microtubule binding region (MTBR) domains of tau adopt a beta-sheet conformation, inducing self-assembly with other tau molecules that lead to the formation of insoluble aggregates. Insoluble tau is also a feature of a number of different neurodegenerative diseases collectively termed tauopathies. The accumulation of insoluble deposits has been suggested to result in altered distribution and function of organelles to adversely affect neuronal cell function as well as causing synapse loss, ultimately leading to cell death. In AD, evidence also suggests a direct correlation between the number of NFTs found in the brain at postmortem and the degree of dementia observed in subjects with AD at the time of death.

The microtubule-associated protein tau (MAPT) gene is located on chromosome 17 of the human genome. Through alternative splicing, 6 possible tau protein isoforms are expressed from this gene in the adult brain. A number of studies have suggested that pathological forms of tau protein transmit from neuron to neuron in human brain to cause disease, including AD. It has also been reported that tau can form seeds, which when applied extracellularly, can cause the initiation and propagation of intracellular tau aggregation. To form tau seeds, the MTBR of the protein is required. Furthermore, the tau MTBR is important in initiating the tau aggregation process and forming the core of fibrils pathologically associated with disease. Together, these observations suggest that therapeutic intervention with an antibody that binds to the MTBR region of tau in the brain, thereby disrupting tau aggregation may prevent initiation or slow down the neurodegeneration in AD or other tauopathies.

Upcoming Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU) trials are designed to investigate therapies targeting tau in combination with amyloid as pre-specified in the approved and NIH-funded NexGen Prevention Trial grants. As with other amyloid lowering drug trials, clinical benefit was not definitively demonstrated in the symptomatic population after tau pathology has been established. Determining the role of tau in disease biology and progression is critically important. Based on beneficial effects on amyloid, tau, and neurodegeneration markers associated with amyloid removal in the gantenerumab trial arm in DIAN-TU, the DIAN-TU will now implement amyloid removal treatment in mutation carriers and add placebo- controlled tau treatment arms. The platform trial design is exceptionally well-suited for the investigation of treatments used in combination because of ongoing multiple arms in a single trial and operational platform.

The current DIAN-TU amyloid removal drug arm has been extended to open-label extension (OLE) periods for prior participants. All enrolled participants who opted-in for OLE were unblinded to genetic status and offered open-label gantenerumab treatment. New treatment- naive mutation positive participants will be started on amyloid removal treatment with genetic counseling and testing. Therefore, all participants will be required to be positive for a dominantly inherited Alzheimer's disease (DIAD) mutation and will receive open-label treatment with lecanemab, an investigational amyloid removal drug, in combination with E2814, an anti-tau drug or placebo. Mutation non-carriers will not be enrolled. Specifically, all E2814 blinded drug arm participants will be treated with the lecanemab and randomized to either active E2814 tau therapy, or placebo.

The goal of the study is to investigate potential benefits of anti-tau therapy while anti-amyloid treatment is given as a background therapy. Furthermore, from ethical and participant recruitment perspectives, launching drug trials using amyloid and tau targeting therapies in combination may be essential, as participants and their families have expressed the need to have a drug that changes amyloid disease pathology in addition to being randomized to an investigational anti-tau drug (E2814) with uncertain benefit.

This record represents an analysis study portion of the Master Protocol Research Program (MPRP) under NCT01760005

Study Design

• Study Type: Interventional (Clinical Trial)
• Estimated Enrollment: 168 participants
• Allocation: Randomized
• Intervention Model: Parallel Assignment
• Intervention Model Description: Interventional
• Masking: Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)
• Primary Purpose: Treatment
• Official Title: A Phase II/III Multicenter Randomized, Double-Blind, Placebo-Controlled Platform Trial of Potential Disease Modifying Therapies Utilizing Biomarker, Cognitive, and Clinical Endpoints in Dominantly Inherited Alzheimer's Disease
• Actual Study Start Date: December 22, 2021
• Estimated Primary Completion Date: July 2027
• Estimated Study Completion Date: October 2027

Arms and Interventions

Arm	Intervention/treatment
Experimental: E2814 plus lecanemab; Symptomatic Population (Cohort 1) At Week 0, participants will receive open-label lecanemab administered intravenously for the full treatment period. At Week 24, participants randomized to E2814 will receive intravenously in a blinded fashion for the remainder of their treatment period. Asymptomatic Population (Cohort 2) At Week 0, participants randomized to E2814 will receive intravenously in a blinded fashion for the full treatment period. At Week 52, all participants will initiate open-label lecanemab administered intravenously for the remainder of their treatment period.	Drug: E2814; Administered intravenously in a blinded fashion; Drug: Lecanemab; Administered intravenously; Other Name: BAN2401
Placebo Comparator: Matching placebo (E2814) plus lecanemab; Symptomatic Population (Cohort 1) At Week 0, participants will receive open-label lecanemab administered intravenously for the full treatment period. At Week 24, participants randomized to E2814 placebo will receive placebo intravenously in a blinded fashion for the remainder of their treatment period. Asymptomatic Population (Cohort 2) At Week 0, participants randomized to E2814 placebo will receive placebo intravenously in a blinded fashion for the full treatment period. At Week 52, all participants will initiate open-label lecanemab administered intravenously for the remainder of their treatment period.	Drug: Lecanemab; Administered intravenously; Other Name: BAN2401; Drug: Matching Placebo (E2814); Placebo administered intravenously in a blinded fashion.

Outcome Measures

Primary Outcome Measures :

1. The primary end point is the change from Week 24 to Week 104 and Week 208 in tau PET in the Symptomatic Population (Cohort 1). [ Time Frame: Weeks 24, 104, and 208 ]
   To determine whether E2814 is superior to placebo, when each is concurrently administered with lecanemab, in the change from Week 24 to Week 104 (interim analysis) and Week 208 (final analysis) in tau spread as measured by tau PET in the symptomatic population (Cohort 1).

Secondary Outcome Measures :

1. Symptomatic Population (Cohort 1): Key Secondary: Change from Week 24 to Week 208 in Clinical Dementia Scale - Sum of Boxes (CDR-SB). [ Time Frame: Weeks 24, 52, 104, 156 and 208 ]

   To determine whether E2814 is superior to placebo, when each is concurrently administered with lecanemab, in change from Week 24 to Week 208 in CDR-SB

   Scores range from 0-18 with lower scores showing better outcomes

2. Asymptomatic Population (Cohort 2): Key Secondary: Change from Week 0 to Week 104 and Week 208 in CSF ptau217/total tau [ Time Frame: Weeks 0, 104 and 208 ]
   To determine whether E2814 is superior to placebo, when each is administered alone and then concurrently with lecanemab, in change from Week 0 to Week 104 (interim analysis) and Week 208 (final analysis) in cerebrospinal fluid (CSF) phosphorylated tau (ptau217)/total tau
3. Symptomatic Population (Cohort 1): Change from Week 24 to Week 104 and Week 208 in the cognitive composite score [ Time Frame: Weeks 24, 52, 76, 104, 128, 156, 180 and 208 ]
4. Symptomatic Population (Cohort 1): Change from Week 0 to Week 24 in amyloid PET [ Time Frame: Week 0 to Week 24 ]
5. Asymptomatic Population (Cohort 2): Change from Week 0 to Week 52 in CSF ptau217/total tau [ Time Frame: Week 0 to Week 52 ]
6. Symptomatic population (Cohort 1): Change from Week 24 to Week 104 and Week 208 in CSF neurofilament light chain (NfL) [ Time Frame: Weeks 24, 104 and 208 ]
7. Asymptomatic Population (Cohort 2): Change from Week 52 to Week 104 and Week 208 in CSF neurofilament light chain (NfL) [ Time Frame: Weeks 52, 104 and 208 ]

Eligibility Criteria

• Ages Eligible for Study: 18 Years to 80 Years (Adult, Older Adult)
• Sexes Eligible for Study: All
• Accepts Healthy Volunteers: No

Criteria

Key Inclusion Criteria:

• Between 18-80 years of age
• Individuals who know they have an Alzheimer's disease-causing mutation.
• Are within -10 to + 10 years of the predicted or actual age of cognitive symptom onset.
• Cognitively normal or with mild cognitive impairment or mild dementia, Clinical Dementia Rating (CDR) of 0-1 (inclusive)
• Fluency in DIAN-TU trial approved language and evidence of adequate premorbid intellectual functioning
• Able to undergo Magnetic Resonance Imaging (MRI), Lumbar Puncture (LP), Positron Emission Tomography (PET), and complete all study related testing and evaluations.
• For women of childbearing potential, if partner is not sterilized, participant must agree to use effective contraceptive measures (hormonal contraception, intra-uterine device, sexual abstinence, barrier method with spermicide).
• Adequate visual and auditory abilities to perform all aspects of the cognitive and functional assessments.
• Has a Study Partner who in the investigator's judgment is able to provide accurate information as to the subject's cognitive and functional abilities, who agrees to provide information at the study visits which require informant input for scale completion.

Key Exclusion Criteria:

• Significant neurologic disease (other than AD) or psychiatric disease that may currently or during the course of the study affect cognition or participant's ability to complete the study.
• At high risk for suicide, e.g., significant suicidal ideation or attempt within last 12 months. Current stable mild depression or current use of antidepressant medications is not exclusionary.
• History or presence of brain MRI scans indicative of any other significant abnormality
• Substance or alcohol use disorder currently or within the past 1 year
• Presence of pacemakers, aneurysm clips, artificial heart valves, ear implants, or foreign metal objects in the eyes, skin or body which would preclude MRI scan.
• History or presence of clinically significant cardiovascular disease, hepatic/renal disorders, infectious disease or immune disorder, or metabolic/endocrine disorders
• Anticoagulants except low dose (≤ 325 mg) aspirin.
• Have been exposed to a monoclonal antibody targeting beta amyloid peptide within the past six months.
• History of cancer within the last 5 years, except basal cell carcinoma, non-squamous skin carcinoma, prostate cancer or carcinoma in situ with no significant progression over the past 2 years.
• Positive urine or serum pregnancy test or plans or desires to become pregnant during the course of the trial.
• Subjects unable to complete all study related testing, including implanted metal that cannot be removed for MRI scanning, required anticoagulation and pregnancy.

Contacts and Locations

Contacts

Contact: Ellen Ziegemeier, MA; 844-DIANEXR (342-6397); dianexr@wustl.edu

Contact: Jamie Bartzel; 844-DIANEXR (342-6397); dianexr@wustl.edu

Locations

United States, Alabama

University of Alabama in Birmingham; Recruiting

Birmingham, Alabama, United States, 35294

Principal Investigator: Erik Roberson

United States, California

University of California San Diego Medical Center; Recruiting

La Jolla, California, United States, 92037

Principal Investigator: Doug Galasko

USC Keck School of Medicine; Recruiting

Los Angeles, California, United States, 90033

Principal Investigator: Sonia Pawluczyk

United States, Connecticut

Yale University School of Medicine; Recruiting

New Haven, Connecticut, United States, 06510

Principal Investigator: Christopher Van Dyck

United States, Georgia

Emory University; Recruiting

Atlanta, Georgia, United States, 30329

Principal Investigator: James Lah

United States, Illinois

Advocate Lutheran General Hospital; Recruiting

Park Ridge, Illinois, United States, 60068

Principal Investigator: Darren Gitelman

United States, Indiana

Indiana University School of Medicine; Recruiting

Indianapolis, Indiana, United States, 46202

Principal Investigator: Jared Brosch

United States, Missouri

Washington University in St. Louis; Recruiting

Saint Louis, Missouri, United States, 63110

Principal Investigator: Barbara Snider

United States, Pennsylvania

University of Pittsburgh; Recruiting

Pittsburgh, Pennsylvania, United States, 15213

Principal Investigator: Sarah Berman

United States, Rhode Island

Butler Hospital; Recruiting

Providence, Rhode Island, United States, 02096

Principal Investigator: Ghulam Surti

United States, Texas

Kerwin Research Center,; Recruiting

Dallas, Texas, United States, 75231

Principal Investigator: Diana Kerwin

United States, Washington

University of Washington; Recruiting

Seattle, Washington, United States, 98195

Principal Investigator: Suman Jayadev

Argentina

Instituto de Investigaciones Neurologicas Raul Carrea, FLENI; Recruiting

Ciudad Autonoma de Buenos Aire, Argentina, C1428AQK

Principal Investigator: Ricardo Allegri

Australia, New South Wales

Neuroscience Research Australia; Recruiting

Randwick, New South Wales, Australia, 2031

Principal Investigator: William Brooks

Australia, Victoria

Mental Health Research Institute; Recruiting

Melbourne, Victoria, Australia, 3010

Principal Investigator: Colin Masters

Brazil

Hospital das Clínicas da Faculdade de Medicina da USP; Recruiting

São Paulo, Brazil, 05403-000

Principal Investigator: Ricardo Nitrini

Canada, British Columbia

UBC Hospital; Recruiting

Vancouver, British Columbia, Canada, V6T 2B5

Principal Investigator: Robin Hsiung

Canada, Ontario

Sunnybrook Health Sciences Centre; Recruiting

Toronto, Ontario, Canada, M4N 3M5

Principal Investigator: Mario Masellis

Canada, Quebec

McGill Center for Studies in Aging; Recruiting

Verdun, Quebec, Canada, H4H 1R3

Principal Investigator: Pedro Rosa-Neto

Canada

CHU de Quebec - Hôpital de l' Enfant Jésus; Recruiting

Québec, Canada, G1J 1Z4

Principal Investigator: Robert LaForce

Colombia

Grupo de Neurociencias Sede de la Universidad de Antioquia; Recruiting

Medellín, Colombia

Principal Investigator: Francisco Lopera, M.D.

France

CHU de Toulouse - Hôpital Purpan; Active, not recruiting

Toulouse, Haute Garonne, France, 31059

Hopital Roger Salengro - CHU Lille; Active, not recruiting

Lille, Nord, France, 59037

Groupe Hospitalier Pitie-Salpetriere; Active, not recruiting

Paris cedex 13, Paris, France, 69677

Hopital Neurologique Pierre Wertheimer; Active, not recruiting

Bron cedex, Rhone, France, 69677

CHU de Rouen - Hôpital Charles Nicolle; Active, not recruiting

Rouen, Seine Maritime, France, 76031

Germany

Universitaetsklinikum Tubingen; Recruiting

Tübingen, Baden Wuerttemberg, Germany, 72076

Principal Investigator: Cristoph Laske, M.D.

LMU-Campus Grosshadern; Recruiting

Muenchen, Bayern, Germany, 81377

Principal Investigator: Johannes Levin, M.D,

Ireland

St Vincent's University Hospital; Active, not recruiting

Dublin, Ireland, DUBLIN 4

Italy

IRCCS Centro San Giovanni di Dio Fatebenefratelli; Recruiting

Brescia, Italy, 25125

Principal Investigator: Giovanni Frisoni, M.D,

Azienda Ospedaliera Universitaria Careggi; Recruiting

Firenze, Italy, 50134

Principal Investigator: Sandro Sorbi, M.D.

Japan

Niigata University Medical & Dental Hospital; Recruiting

Niigata-shi, Niigata-Ken, Japan, 951-8520

Contact: M.D.

Principal Investigator: Kensaku Kasuga, M.D.

University of Tokyo Hospital; Recruiting

Bunkyō-Ku, Tokyo-To, Japan, 113-8655

Principal Investigator: Yoshiki Niimi, M.D.

Mexico

Instituto Nacional de Neurologia y Neurocirugia Manuel Velasco Suarez; Active, not recruiting

Mexico, Distrito Federal, Mexico, 14269

Netherlands

Brain Research Center; Recruiting

Amsterdam, Netherlands, 1081 GM

Principal Investigator: Phillip Scheltens, MD

Puerto Rico

University of Puerto Rico, School of Medicine; Recruiting

San Juan, Puerto Rico, 00936

Principal Investigator: Ivonne Jimenez-Velazquez

Spain

Hospital Clínic I Provincial de Barcelona; Recruiting

Barcelona, Spain, 8036

Principal Investigator: Raquel Sanchez Valle

United Kingdom

The National Hospital for Neurology and Neurosurgery; Recruiting

London, Greater London, United Kingdom, WC1B 3BG

Principal Investigator: Catherine Mummery

Sponsors and Collaborators

Washington University School of Medicine

Alzheimer's Association

National Institute on Aging (NIA)

Accelerating Medicines Partnership (AMP)

Eisai Inc.

Investigators

• Study Director: Randall J Bateman, MD; Washington University School of Medicine

More Information

Additional Information:

Expanded registry 

Publications:

Jack CR Jr, Knopman DS, Jagust WJ, Petersen RC, Weiner MW, Aisen PS, Shaw LM, Vemuri P, Wiste HJ, Weigand SD, Lesnick TG, Pankratz VS, Donohue MC, Trojanowski JQ. Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 2013 Feb;12(2):207-16. doi: 10.1016/S1474-4422(12)70291-0.

Fitzpatrick AWP, Falcon B, He S, Murzin AG, Murshudov G, Garringer HJ, Crowther RA, Ghetti B, Goedert M, Scheres SHW. Cryo-EM structures of tau filaments from Alzheimer's disease. Nature. 2017 Jul 13;547(7662):185-190. doi: 10.1038/nature23002. Epub 2017 Jul 5.

Falcon B, Zhang W, Murzin AG, Murshudov G, Garringer HJ, Vidal R, Crowther RA, Ghetti B, Scheres SHW, Goedert M. Structures of filaments from Pick's disease reveal a novel tau protein fold. Nature. 2018 Sep;561(7721):137-140. doi: 10.1038/s41586-018-0454-y. Epub 2018 Aug 29.

Kopeikina KJ, Hyman BT, Spires-Jones TL. Soluble forms of tau are toxic in Alzheimer's disease. Transl Neurosci. 2012 Sep;3(3):223-233. doi: 10.2478/s13380-012-0032-y.

Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol. 1991;82(4):239-59. doi: 10.1007/BF00308809.

Goedert M, Spillantini MG. Propagation of Tau aggregates. Mol Brain. 2017 May 30;10(1):18. doi: 10.1186/s13041-017-0298-7.

Falcon B, Cavallini A, Angers R, Glover S, Murray TK, Barnham L, Jackson S, O'Neill MJ, Isaacs AM, Hutton ML, Szekeres PG, Goedert M, Bose S. Conformation determines the seeding potencies of native and recombinant Tau aggregates. J Biol Chem. 2015 Jan 9;290(2):1049-65. doi: 10.1074/jbc.M114.589309. Epub 2014 Nov 18.

Barghorn S, Zheng-Fischhofer Q, Ackmann M, Biernat J, von Bergen M, Mandelkow EM, Mandelkow E. Structure, microtubule interactions, and paired helical filament aggregation by tau mutants of frontotemporal dementias. Biochemistry. 2000 Sep 26;39(38):11714-21. doi: 10.1021/bi000850r.

von Bergen M, Friedhoff P, Biernat J, Heberle J, Mandelkow EM, Mandelkow E. Assembly of tau protein into Alzheimer paired helical filaments depends on a local sequence motif ((306)VQIVYK(311)) forming beta structure. Proc Natl Acad Sci U S A. 2000 May 9;97(10):5129-34. doi: 10.1073/pnas.97.10.5129.

von Bergen M, Barghorn S, Li L, Marx A, Biernat J, Mandelkow EM, Mandelkow E. Mutations of tau protein in frontotemporal dementia promote aggregation of paired helical filaments by enhancing local beta-structure. J Biol Chem. 2001 Dec 21;276(51):48165-74. doi: 10.1074/jbc.M105196200. Epub 2001 Oct 17.

Salloway S, Farlow M, McDade E, Clifford DB, Wang G, Llibre-Guerra JJ, Hitchcock JM, Mills SL, Santacruz AM, Aschenbrenner AJ, Hassenstab J, Benzinger TLS, Gordon BA, Fagan AM, Coalier KA, Cruchaga C, Goate AA, Perrin RJ, Xiong C, Li Y, Morris JC, Snider BJ, Mummery C, Surti GM, Hannequin D, Wallon D, Berman SB, Lah JJ, Jimenez-Velazquez IZ, Roberson ED, van Dyck CH, Honig LS, Sanchez-Valle R, Brooks WS, Gauthier S, Galasko DR, Masters CL, Brosch JR, Hsiung GR, Jayadev S, Formaglio M, Masellis M, Clarnette R, Pariente J, Dubois B, Pasquier F, Jack CR Jr, Koeppe R, Snyder PJ, Aisen PS, Thomas RG, Berry SM, Wendelberger BA, Andersen SW, Holdridge KC, Mintun MA, Yaari R, Sims JR, Baudler M, Delmar P, Doody RS, Fontoura P, Giacobino C, Kerchner GA, Bateman RJ; Dominantly Inherited Alzheimer Network-Trials Unit. A trial of gantenerumab or solanezumab in dominantly inherited Alzheimer's disease. Nat Med. 2021 Jul;27(7):1187-1196. doi: 10.1038/s41591-021-01369-8. Epub 2021 Jun 21.

Sandusky-Beltran LA, Sigurdsson EM. Tau immunotherapies: Lessons learned, current status and future considerations. Neuropharmacology. 2020 Sep 15;175:108104. doi: 10.1016/j.neuropharm.2020.108104. Epub 2020 Apr 28.

• Responsible Party: Washington University School of Medicine
• ClinicalTrials.gov Identifier: NCT05269394
• Other Study ID Numbers: DIAN-TU-001 (E2814); The Alzheimer's Association ( Other Grant/Funding Number: DIAN TTU-12-243040 ); U01AG042791 ( U.S. NIH Grant/Contract ); 2013-000307-17 ( EudraCT Number ); R01AG046179 ( U.S. NIH Grant/Contract ); REec-2014-0817 ( Registry Identifier: Spanish Clinical Studies Registry ); The Alzheimer's Association ( Other Grant/Funding Number: DIAN-TU Tau-15-347219 ); GHR Foundation ( Other Grant/Funding Number: File 4401 ); Alzheimer's Association ( Other Identifier: HDE 18S84914 ); The Alzheimer's Association ( Other Grant/Funding Number: DIAN-TU NG-16-434362 ); R56AG053267 ( U.S. NIH Grant/Contract ); U01AG059798 ( U.S. NIH Grant/Contract ); R01AG053267 ( U.S. NIH Grant/Contract ); R01AG068319 ( U.S. NIH Grant/Contract ); The Alzheimer's Association ( Other Grant/Funding Number: DIAN-TU Tau-21822987 ); The Alzheimer's Association ( Other Identifier: DIAN-TU OLE-21725093 )
• First Posted: March 8, 2022
• Last Update Posted: February 22, 2024
• Last Verified: February 2024

Individual Participant Data (IPD) Sharing Statement:

• Plan to Share IPD: Yes
• Plan Description: Access to DIAN-TU trial data will follow the DIAN-TU data access policy, which complies with the guidelines established by the Collaboration for Alzheimer's Prevention [CAP REF].

• Studies a U.S. FDA-regulated Drug Product: Yes
• Studies a U.S. FDA-regulated Device Product: No

Keywords provided by Washington University School of Medicine:

Alzheimer's; Alzheimer's Disease; Dementia; Mutation; Genetic Mutation; Dominantly Inherited Alzheimer's Disease; Dominantly Inherited Alzheimer Network; Autosomal Dominant Alzheimer's Disease; Early Onset Alzheimer's Disease; DIAN; DIAN-TU; DIAN TU; DIAD

Additional relevant MeSH terms:

Alzheimer Disease; Dementia; Brain Diseases; Central Nervous System Diseases; Nervous System Diseases; Tauopathies; Neurodegenerative Diseases; Neurocognitive Disorders; Mental Disorders