New approaches to symptomatic treatments for Alzheimer’s disease

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Abstract

Background

Successful development of agents that improve cognition and behavior in Alzheimer’s disease (AD) is critical to improving the lives of patients manifesting the symptoms of this progressive disorder.

Discussion

There have been no recent approvals of cognitive enhancing agents for AD. There are currently 6 cognitive enhancers in Phase 2 trials and 4 in phase 3. They represent a variety of novel mechanisms. There has been progress in developing new treatments for neuropsychiatric symptoms in AD with advances in treatment of insomnia, psychosis, apathy, and agitation in AD. There are currently 4 AD-related psychotropic agents in Phase 2 trials and 7 in Phase 3 trials. Many novel mechanisms are being explored for the treatment of cognitive and behavioral targets. Progress in trial designs, outcomes measures, and population definitions are improving trial conduct for symptomatic treatment of AD.

Conclusions

Advances in developing new agents for cognitive and behavioral symptoms of AD combined with enhanced trial methods promise to address the unmet needs of patients with AD for improved cognition and amelioration of neuropsychiatric symptoms.

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Most cited references 127

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Neuroinflammation in Alzheimer's disease.

Michael T Heneka, Monica Carson, Joseph El Khoury … (2015)

Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

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Alzheimer's disease.

Philip Scheltens, Kaj Blennow, Monique Breteler … (2016)

Although the prevalence of dementia continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health. Alzheimer's disease, the most prevalent cause of dementia, is still defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality as proposed in the original amyloid hypothesis. Age-related, protective, and disease-promoting factors probably interact with the core mechanisms of the disease. Amyloid β42, and tau proteins are established core cerebrospinal biomarkers; novel candidate biomarkers include amyloid β oligomers and synaptic markers. MRI and fluorodeoxyglucose PET are established imaging techniques for diagnosis of Alzheimer's disease. Amyloid PET is gaining traction in the clinical arena, but validity and cost-effectiveness remain to be established. Tau PET might offer new insights and be of great help in differential diagnosis and selection of patients for trials. In the search for understanding the disease mechanism and keys to treatment, research is moving increasingly into the earliest phase of disease. Preclinical Alzheimer's disease is defined as biomarker evidence of Alzheimer's pathological changes in cognitively healthy individuals. Patients with subjective cognitive decline have been identified as a useful population in whom to look for preclinical Alzheimer's disease. Moderately positive results for interventions targeting several lifestyle factors in non-demented elderly patients and moderately positive interim results for lowering amyloid in pre-dementia Alzheimer's disease suggest that, ultimately, there will be a future in which specific anti-Alzheimer's therapy will be combined with lifestyle interventions targeting general brain health to jointly combat the disease. In this Seminar, we discuss the main developments in Alzheimer's research.

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Author and article information

Contributors

Jeffrey Cummings:

ORCID: http://orcid.org/0000-0001-8944-4158

jcummings@cnsinnovations.com

Journal

Journal ID (nlm-ta): Mol Neurodegener

Journal ID (iso-abbrev): Mol Neurodegener

Title: Molecular Neurodegeneration

Publisher: BioMed Central (London )

ISSN (Electronic): 1750-1326

Publication date (Electronic): 13 January 2021

Publication date PMC-release: 13 January 2021

Publication date Collection: 2021

Volume: 16

Electronic Location Identifier: 2

Affiliations

GRID grid.272362.0, ISNI 0000 0001 0806 6926, Chambers-Grundy Center for Transformative Neuroscience, Department of Brain Health, , School of Integrated Health Sciences, University of Nevada Las Vegas, ; Las Vegas, NV USA

Author notes

For: “AD: Challenges for the Next Decade”, organized by Drs. Todd Golde, Alison Goate, and Guojun Bu as the lead editors. The series is to be published in Molecular Neurodegeneration in 2020-2021.

Author information

Jeffrey Cummings http://orcid.org/0000-0001-8944-4158

Article

Publisher ID: 424

DOI: 10.1186/s13024-021-00424-9

PMC ID: 7805095

PubMed ID: 33441154

SO-VID: 2b5491a6-5830-4841-a880-80f5a9bb8982

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 26 August 2020

Date accepted : 2 January 2021

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000057, National Institute of General Medical Sciences;

Award ID: P20GM109025

Award Recipient : Jeffrey Cummings

Funded by: FundRef http://dx.doi.org/10.13039/100000065, National Institute of Neurological Disorders and Stroke;

Award ID: U01NS093334

Award Recipient : Jeffrey Cummings

Funded by: FundRef http://dx.doi.org/10.13039/100000049, National Institute on Aging;

Award ID: R01AG053798

Award Recipient : Jeffrey Cummings

Custom metadata

ScienceOpen disciplines: Neurosciences

Keywords: neuropsychiatry,alzheimer’s disease,psychosis,apathy,agitation,depression,drug development,clinical trials,cognition

Data availability:

ScienceOpen disciplines: Neurosciences

Keywords: neuropsychiatry, alzheimer’s disease, psychosis, apathy, agitation, depression, drug development, clinical trials, cognition

New approaches to symptomatic treatments for Alzheimer’s disease

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Abstract

Background

Discussion

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Alternative approaches to Alzheimer's Disease

Most cited references 127

"Mini-mental state". A practical method for grading the cognitive state of patients for the clinician.

Neuroinflammation in Alzheimer's disease.

Alzheimer's disease.

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