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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...

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Related Experiment Video

Updated: May 9, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Immunotherapy for Alzheimer's disease.

Martin R Farlow¹, Jared R Brosch

¹Department of Neurology, Indiana University School of Medicine, 355 West 16th Street, Suite 4700, Indianapolis, IN 46202, USA. mfarlow@iupui.edu

Neurologic Clinics

|July 31, 2013

Summary

Immunotherapies targeting amyloid in Alzheimer disease (AD) have shown limited success and adverse events. Future research should focus on earlier intervention and precise targeting of immune responses in AD.

Keywords:

Alzheimer disease Immunotherapy β-amyloid

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Last Updated: May 9, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Area of Science:

Neuroimmunology
Alzheimer Disease Pathogenesis

Background:

The immune system is implicated in Alzheimer disease (AD) pathogenesis.
Amyloid-beta (Aβ) deposition is an early event, and the amyloid hypothesis suggests its removal may slow progression.
Current immunotherapies targeting amyloid have yielded disappointing results in symptomatic patients.

Purpose of the Study:

To evaluate the efficacy and safety of immunotherapies in Alzheimer disease.
To explore the role of the immune system in AD progression.
To identify optimal strategies for future AD immunotherapies.

Main Methods:

Review of human clinical trials involving active or passive immune agents targeting amyloid.
Analysis of adverse events associated with these immunotherapies.
Consideration of disease stage at the time of intervention.

Main Results:

Human trials of immune agents for AD have not demonstrated significant clinical benefit.
Adverse events, including vasogenic edema and microhemorrhages, were observed.
Disease progression may be too advanced by the time dementia symptoms appear.

Conclusions:

Current immunotherapy approaches for Alzheimer disease require re-evaluation.
Targeting immunotherapies requires a better understanding of their precise mechanisms and optimal timing.
Earlier intervention and refined therapeutic strategies are crucial for future Alzheimer disease treatment.