Related Experiment Video
Updated: Jun 10, 2026

15:23
Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease
Published on: May 14, 2010
Amyloid-beta immunisation for Alzheimer's disease
Thomas Wisniewski1, Uwe Konietzko
1Department of Neurology, New York University School of Medicine, New York, NY 10016, USA. thomas.wisniewski@nyumc.org
The Lancet. Neurology
|August 1, 2008
Summary
Alzheimer's disease treatments are lacking. Research focuses on immunotherapy to target toxic amyloid-beta (Abeta) forms, aiming to prevent its conversion and clear existing aggregates.
Area of Science:
- Neuroscience
- Immunology
- Gerontology
Background:
- Alzheimer's disease (AD) is a leading cause of dementia in aging populations.
- Current treatments for AD do not halt or effectively modify disease progression.
- Pathological conversion of amyloid-beta (Abeta) peptide into neurotoxic oligomers is central to AD pathogenesis.
Purpose of the Study:
- To review current immunological approaches for Alzheimer's disease.
- To highlight the development of novel immunotherapies targeting Abeta.
- To discuss the challenges in balancing Abeta clearance with autoimmune reactions.
Main Methods:
- Review of ongoing clinical trials for active and passive immunotherapies.
- Analysis of immunological strategies to prevent Abeta conversion and aggregation.
- Examination of the neurotoxic mechanisms of Abeta oligomers.
Main Results:
- Over ten new active and passive immunotherapy strategies are in clinical trials for AD.
- Immunological approaches aim to prevent pathological Abeta formation and enhance clearance.
- Smallest neurotoxic Abeta species, such as dimers and oligomers, are key targets.
Conclusions:
- Developing safe and effective immunotherapies for Alzheimer's disease is a critical unmet need.
- Targeting amyloid-beta offers a promising therapeutic avenue for Alzheimer's disease.
- Careful modulation of the immune response is essential to avoid adverse effects while clearing toxic Abeta.
Related Concept Videos
Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Alzheimer's Disease: Overview
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer's Disease: Treatment
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...

