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Updated: May 4, 2026

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Alzheimer's disease: new data highlight nonneuronal cell types and the necessity for presymptomatic prevention
1Departments of Neurology and Psychiatry, and the Mount Sinai Alzheimer's Disease Research Center, Icahn School of Medicine at Mount Sinai, and James J. Peters VA Medical Center, New York, New York.
Abstract:
Despite compelling genetic evidence indicating that cerebral amyloidosis can be, at least sometimes, the primary cause of Alzheimer's disease (AD), clinical trials for symptomatic AD with amyloid-reducing agents have succeeded at target engagement but failed to cause clinical benefit. In a landmark shift, the U.S. Food and Drug Administration now proposes to approve prophylaxis that alters the trajectory of what is now believed to be typical AD biomarker evolution. The first prevention trials are now beginning in patients with genetic guarantees for or high genetic risks for AD. The expectation is that clues to their outcomes will begin to emerge from these trials in approximately 2018. In the meantime, new strategies point to nonneuronal cells and to system pathology. A review of the current state of the art of AD science follows herein.
Insights
Alzheimer's disease (AD) prevention trials are shifting focus to early intervention, altering biomarker evolution before symptoms appear. New strategies explore nonneuronal cells and systemic pathology for AD treatment.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Compelling genetic evidence suggests cerebral amyloidosis can be a primary cause of Alzheimer's disease (AD).
- Clinical trials targeting symptomatic AD with amyloid-reducing agents achieved target engagement but lacked clinical benefit.
- A paradigm shift is occurring, with regulatory bodies considering prophylaxis to alter AD biomarker evolution.
Purpose of the Study:
- To review the current state of Alzheimer's disease (AD) science.
- To discuss the implications of a landmark shift towards preventative strategies for AD.
- To highlight emerging research directions focusing on nonneuronal cells and systemic pathology.
Main Methods:
- Review of current scientific literature and clinical trial data on Alzheimer's disease (AD).
- Analysis of genetic evidence linking cerebral amyloidosis to AD pathogenesis.
- Examination of emerging therapeutic strategies beyond traditional amyloid-targeting agents.
Main Results:
- Amyloid-reducing agents have shown efficacy in target engagement but not clinical benefit for symptomatic AD.
- The U.S. FDA is proposing approval for prophylaxis aimed at altering AD biomarker trajectories.
- Prevention trials are commencing in individuals at high genetic risk for AD.
Conclusions:
- The field of Alzheimer's disease (AD) is moving towards early intervention and prevention.
- Future AD research is exploring novel targets including nonneuronal cells and systemic pathology.
- Outcomes from ongoing prevention trials are anticipated to provide crucial insights into AD's trajectory.
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