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Review
. 2022 Sep 14;10(9):1527.
doi: 10.3390/vaccines10091527.

Immunotherapies for Alzheimer's Disease-A Review

Zachary Valiukas  1 , Ramya Ephraim  2 , Kathy Tangalakis  3   4 , Majid Davidson  2   5 , Vasso Apostolopoulos  2   5 , Jack Feehan  2   5
Affiliations
Review

Immunotherapies for Alzheimer's Disease-A Review

Zachary Valiukas et al. Vaccines (Basel). .

Abstract

Alzheimer's disease (AD) is a chronic neurodegenerative disorder that falls under the umbrella of dementia and is characterised by the presence of highly neurotoxic amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) of tau protein within the brain. Historically, treatments for AD have consisted of medications that can slow the progression of symptoms but not halt or reverse them. The shortcomings of conventional drugs have led to a growing need for novel, effective approaches to the treatment of AD. In recent years, immunotherapies have been at the forefront of these efforts. Briefly, immunotherapies utilise the immune system of the patient to treat a condition, with common immunotherapies for AD consisting of the use of monoclonal antibodies or vaccines. Most of these treatments target the production and deposition of Aβ due to its neurotoxicity, but treatments specifically targeting tau protein are being researched as well. These treatments have had great variance in their efficacy and safety, leading to a constant need for the research and development of new safe and effective treatments.

Keywords: Alzheimer’s disease; amyloid-beta; dementia; immunotherapies; vaccines.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Pathophysiological differences between a healthy and an AD brain. Tissue degeneration is highly prevalent. Neuronal degeneration to Aβ and NFTs is highlighted. Created with BioRender.com.
Figure 2
Figure 2
Generation of Aβ from APP. APP is cleaved by BACE-1 to generate C99 and is then cleaved again by γ-secretase to generate free A-beta. Created with BioRender.com.
Figure 3
Figure 3
Glial- and astrocyte-mediated neuroinflammation related to AD. Both microglial and astrocyte-mediated pathways result in the release and activation of pro-inflammatory molecules such as IL-1α, IL-6, and TNF-α. Created with BioRender.com.
Figure 4
Figure 4
The general theory for immunotherapy against AD pertaining to Aβ pathophysiology. Antibody therapy involves the administering of antibodies to the patient, active immunotherapy involves using a vaccine to make the patient produce their own. Created with BioRender.com.
See this image and copyright information in PMC

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