» Articles » PMID: 35563389

Stress-Induced Depression and Alzheimer's Disease: Focus on Astrocytes

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2022 May 14
PMID 35563389
Authors
Affiliations
Soon will be listed here.
Abstract

Neurodegenerative diseases and depression are multifactorial disorders with a complex and poorly understood physiopathology. Astrocytes play a key role in the functioning of neurons in norm and pathology. Stress is an important factor for the development of brain disorders. Here, we review data on the effects of stress on astrocyte function and evidence of the involvement of astrocyte dysfunction in depression and Alzheimer's disease (AD). Stressful life events are an important risk factor for depression; meanwhile, depression is an important risk factor for AD. Clinical data indicate atrophic changes in the same areas of the brain, the hippocampus and prefrontal cortex (PFC), in both pathologies. These brain regions play a key role in regulating the stress response and are most vulnerable to the action of glucocorticoids. PFC astrocytes are critically involved in the development of depression. Stress alters astrocyte function and can result in pyroptotic death of not only neurons, but also astrocytes. BDNF-TrkB system not only plays a key role in depression and in normalizing the stress response, but also appears to be an important factor in the functioning of astrocytes. Astrocytes, being a target for stress and glucocorticoids, are a promising target for the treatment of stress-dependent depression and AD.

Citing Articles

Neuroimaging Findings of Psychosis in Alzheimer's Disease: A Systematic Review.

Nabizadeh F, Sheykhlou S, Mahmoodi S, Khalili E, Zafari R, Hosseini H Brain Behav. 2024; 15(1):e70205.

PMID: 39740792 PMC: 11688121. DOI: 10.1002/brb3.70205.


The neural basis of neuropsychiatric symptoms in Alzheimer's disease.

Zhang N, Zhang S, Zhang L, Tao H, Zhang G Front Aging Neurosci. 2024; 16:1487875.

PMID: 39703925 PMC: 11655510. DOI: 10.3389/fnagi.2024.1487875.


The Aggravating Role of Failing Neuropeptide Networks in the Development of Sporadic Alzheimer's Disease.

Jaszberenyi M, Thurzo B, Jayakumar A, Schally A Int J Mol Sci. 2024; 25(23).

PMID: 39684795 PMC: 11641508. DOI: 10.3390/ijms252313086.


Neuroinflammation and major depressive disorder: astrocytes at the crossroads.

Puentes-Orozco M, Albarracin S, Velasquez M Front Cell Neurosci. 2024; 18:1504555.

PMID: 39650796 PMC: 11620873. DOI: 10.3389/fncel.2024.1504555.


Alzheimer's Disease, Obesity, and Type 2 Diabetes: Focus on Common Neuroglial Dysfunctions (Critical Review and New Data on Human Brain and Models).

Toledano A, Rodriguez-Casado A, Alvarez M, Toledano-Diaz A Brain Sci. 2024; 14(11).

PMID: 39595866 PMC: 11591712. DOI: 10.3390/brainsci14111101.


References
1.
Quesseveur G, Portal B, Basile J, Ezan P, Mathou A, Halley H . Attenuated Levels of Hippocampal Connexin 43 and its Phosphorylation Correlate with Antidepressant- and Anxiolytic-Like Activities in Mice. Front Cell Neurosci. 2016; 9:490. PMC: 4686612. DOI: 10.3389/fncel.2015.00490. View

2.
Rajkowska G, Stockmeier C . Astrocyte pathology in major depressive disorder: insights from human postmortem brain tissue. Curr Drug Targets. 2013; 14(11):1225-36. PMC: 3799810. DOI: 10.2174/13894501113149990156. View

3.
Chi S, Yu J, Tan M, Tan L . Depression in Alzheimer's disease: epidemiology, mechanisms, and management. J Alzheimers Dis. 2014; 42(3):739-55. DOI: 10.3233/JAD-140324. View

4.
Brendel M, Sauerbeck J, Greven S, Kotz S, Scheiwein F, Blautzik J . Serotonin Selective Reuptake Inhibitor Treatment Improves Cognition and Grey Matter Atrophy but not Amyloid Burden During Two-Year Follow-Up in Mild Cognitive Impairment and Alzheimer's Disease Patients with Depressive Symptoms. J Alzheimers Dis. 2018; 65(3):793-806. DOI: 10.3233/JAD-170387. View

5.
Lowe Jr W, Meyer T, Karpen C, Lorentzen L . Regulation of insulin-like growth factor I production in rat C6 glioma cells: possible role as an autocrine/paracrine growth factor. Endocrinology. 1992; 130(5):2683-91. DOI: 10.1210/endo.130.5.1572288. View