What is the mechanism of action of this treatment?

The most common treatments for Alzheimer's Disease often target amyloid plaques and tau tangles, which are hallmark features of the disease. Amyloid-targeting therapies, such as aducanumab, work by binding to amyloid-beta plaques in the brain, promoting their clearance and potentially slowing cognitive decline. Tau-targeting treatments aim to prevent the abnormal aggregation of tau proteins, which form tangles that disrupt neuronal function. These mechanisms are crucial as they directly address the pathological processes underlying Alzheimer's, offering hope for slowing disease progression and improving quality of life for patients.

What side effects are associated with this type of intervention?

Common treatments for Alzheimer's Disease, particularly those targeting amyloid plaques such as aducanumab, have several known side effects. Aducanumab can cause amyloid-related imaging abnormalities (ARIA), which include brain swelling and small brain bleeds, reported in approximately 40% of patients at the highest dose. Other side effects include headache, falls, diarrhea, and confusion. Additionally, hypersensitivity reactions like angioedema and urticaria have been observed. These treatments require careful monitoring due to the potential for serious adverse effects.

What prior FDA approvals exist?

The FDA has approved several treatments for Alzheimer's Disease that target amyloid plaques, including aducanumab (Aduhelm), which is a monoclonal antibody designed to reduce amyloid-beta plaques in the brain. Another notable treatment is donepezil, an acetylcholinesterase inhibitor, which, while not directly targeting amyloid plaques or tau tangles, helps improve cognitive function by increasing acetylcholine levels. Additionally, memantine, an NMDA receptor antagonist, is used to manage symptoms by regulating glutamate activity. These treatments represent the current landscape of FDA-approved drugs aimed at modifying disease progression or managing symptoms in Alzheimer's Disease.

What other types of research exist?

One promising novel alternative to investigational Alzheimer's medications targeting amyloid plaques or tau tangles is Trappsol Cyclo, which is currently being evaluated for its safety and potential efficacy in patients with early Alzheimer's disease. This treatment is part of a 6-month study involving approximately 90 patients aged 50 to 80 years. The study includes a screening period, a treatment period, and a follow-up period to assess overall health post-participation.

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Trappsol Cyclo for Early Alzheimer's Disease (EAD501 Trial)

Phase 2

Waitlist Available

Research Sponsored by Cyclo Therapeutics, Inc.

Eligibility Criteria Checklist

Specific guidelines that determine who can or cannot participate in a clinical trial

Must have

Be older than 18 years old

Timeline

Screening 3 weeks

Treatment Varies

Follow Up weeks 4, 8, 12, and 24

Summary

This trial is testing Trappsol Cyclo, a medication, to see if it can help people aged 50 to 80 with early Alzheimer's disease. The study will check if the medication is safe and if it can improve or stabilize their cognitive functions. Participants will receive either the medication or an inactive substance without knowing which one they are getting.

Who is the study for?

This trial is for people aged 50-80 with early Alzheimer's, confirmed by specific cognitive tests and biomarkers. Participants must have stable cognitive scores and no severe hypothyroidism, vitamin B12 deficiency, significant kidney disease, or other neurodegenerative diseases.

What is being tested?

The study compares two doses of Hydroxypropyl Beta Cyclodextrin (Trappsol Cyclo) against a placebo in patients with early Alzheimer's. It involves three phases: screening for eligibility, treatment administration, and follow-up health checks.

What are the potential side effects?

While the side effects are not specified here, common ones may include reactions at the injection site, gastrointestinal issues like nausea or diarrhea, potential liver enzyme elevations or hearing disturbances due to the nature of cyclodextrins.

Timeline

Screening ~ 3 weeks3 visits

Treatment ~ Varies

Follow Up ~ weeks 4, 8, 12, and 24

Screening ~ 3 weeks

Treatment ~ Varies

Follow Up ~weeks 4, 8, 12, and 24

This trial's timeline: 3 weeks for screening, Varies for treatment, and weeks 4, 8, 12, and 24 for reporting.

Treatment Details

Study Objectives

Study objectives can provide a clearer picture of what you can expect from a treatment.

Primary study objectives

Safety assessments to include incidence of Adverse Events and Serious Adverse Events

Secondary study objectives

Change in ADCS-ADL from Baseline

Change in ADCS-CGIC from Baseline

Complementarity Determining Regions

+2 more

Other study objectives

Area under the plasma concentration versus time curve (AUC)

Change in combined Z-scores from Baseline (V2) to Weeks 12 (V5) and 24 (V8) on ADAS-Cog-14

Change in combined Z-scores from Baseline (V2) to Weeks 12 (V5) and 24 (V8) on CDR-SB

+3 more

Trial Design

2Treatment groups

Experimental Treatment

Placebo Group

Group I: ExperimentalExperimental Treatment1 Intervention

Intravenous administration over at least 4 hours by IV infusion Trappsol Cyclo either 500 mg/kg or 1000 mg/kg every 4 weeks

Group II: PlaceboPlacebo Group1 Intervention

Intravenous administration of 0.5N saline over at least 4 hours every 4 weeks

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Research Highlights

Information in this section is not a recommendation. We encourage patients to speak with their healthcare team when evaluating any treatment decision.

Mechanism Of Action

Side Effect Profile

Prior Approvals

Other Research

The most common treatments for Alzheimer's Disease often target amyloid plaques and tau tangles, which are hallmark features of the disease. Amyloid-targeting therapies, such as aducanumab, work by binding to amyloid-beta plaques in the brain, promoting their clearance and potentially slowing cognitive decline. Tau-targeting treatments aim to prevent the abnormal aggregation of tau proteins, which form tangles that disrupt neuronal function. These mechanisms are crucial as they directly address the pathological processes underlying Alzheimer's, offering hope for slowing disease progression and improving quality of life for patients.