Depression—an underrecognized target for prevention of dementia in Alzheimer’s disease

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

It is broadly acknowledged that the onset of dementia in Alzheimer’s disease (AD) may be modifiable by the management of risk factors. While several recent guidelines and multidomain intervention trials on prevention of cognitive decline address lifestyle factors and risk diseases, such as hypertension and diabetes, a special reference to the established risk factor of depression or depressive symptoms is systematically lacking. In this article we review epidemiological studies and biological mechanisms linking depression with AD and cognitive decline. We also emphasize the effects of antidepressive treatment on AD pathology including the molecular effects of antidepressants on neurogenesis, amyloid burden, tau pathology, and inflammation. We advocate moving depression and depressive symptoms into the focus of prevention of cognitive decline and dementia. We constitute that early treatment of depressive symptoms may impact on the disease course of AD and affect the risk of developing dementia and we propose the need for clinical trials.

Related collections

Most cited references 88

Record: found
Abstract: found
Article: found

Dementia prevention, intervention, and care

Gill Livingston, Andrew Sommerlad, Vasiliki Orgeta … (2018)

0 comments Cited 2010 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The role of inflammation in depression: from evolutionary imperative to modern treatment target.

Andrew Miller, Charles L. Raison (2016)

Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.

0 comments Cited 1093 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

A neurotrophic model for stress-related mood disorders.

Ronald S. Duman, Lisa M. Monteggia (2006)

There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies. Although there are some limitations, the results of these studies are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation of BDNF plays a role in the actions of antidepressant treatment.

0 comments Cited 786 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Forugh S. Dafsari: forugh.salimi-dafsari@uk-koeln.de

Journal

Journal ID (nlm-ta): Transl Psychiatry

Journal ID (iso-abbrev): Transl Psychiatry

Title: Translational Psychiatry

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2158-3188

Publication date (Electronic): 20 May 2020

Publication date PMC-release: 20 May 2020

Publication date Collection: 2020

Volume: 10

Electronic Location Identifier: 160

Affiliations

[1 ]ISNI 0000 0000 8852 305X, GRID grid.411097.a, Department of Psychiatry and Psychotherapy, University of Cologne, , Faculty of Medicine and University Hospital Cologne, ; Kerpener Straße 62, 50937 Cologne, Germany

[2 ]ISNI 0000 0004 4911 0702, GRID grid.418034.a, Max-Planck-Institute for Metabolism Research, ; Gleueler Str. 50, 50931 Cologne, Germany

[3 ]ISNI 0000 0004 0438 0426, GRID grid.424247.3, German Center for Neurodegenerative Disease (DZNE), ; Sigmund-Freud-Str. 27, 53127 Bonn, Germany

Article

Publisher ID: 839

DOI: 10.1038/s41398-020-0839-1

PMC ID: 7239844

PubMed ID: 32433512

SO-VID: bee46d20-f3d9-4b69-9b8a-bfd1bf89464d

License:

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.