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Parallels Between Major Depressive Disorder and Alzheimer’s Disease: Role of Oxidative Stress and Genetic Vulnerability

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Abstract

The thesis of this review is that oxidative stress is the central factor in major depressive disorder (MDD) and Alzheimer’s disease (AD). The major elements involved are inflammatory cytokines, the hypothalamic–pituitary axis, the hypothalamic–pituitary gonadal, and arginine vasopressin systems, which induce glucocorticoid and “oxidopamatergic” cascades when triggered by psychosocial stress, severe life-threatening events, and mental-affective and somatic diseases. In individuals with a genomic vulnerability to depression, these cascades may result in chronic depression–anxiety–stress spectra, resulting in MDD and other known depressive syndromes. In contrast, in subjects with genomic vulnerability to AD, oxidative stress-induced brain damage triggers specific antioxidant defenses, i.e., increased levels of amyloid-β (Aβ) and aggregation of hyper-phosphorylated tau, resulting in paired helical filaments and impaired functions related to the ApoEε4 isoform, leading to complex pathological cascades culminating in AD. Surprisingly, all the AD-associated molecular pathways mentioned in this review have been shown to be similar or analogous to those found in depression, including structural damage, i.e., hippocampal and frontal cortex atrophy. Other interacting molecular signals, i.e., GSK-3β, convergent survival factors (brain-derived neurotrophic factor and heat shock proteins), and transition redox metals are also mentioned to emphasize the vast array of intermediates that could interact via comparable mechanisms in both MDD and AD.

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Abbreviations

AD:

Alzheimer’s disease

Aβ:

Amyloid-β

ACTH:

Adrenal corticotrophic hormone

AGE:

Advanced glycation end product

ApoEε4:

Apolipoprotein Eε4

AβPP:

Amyloid β protein precursor

BDNF:

Brain-derived neurotrophic factor

CSF:

Cerebral spinal fluid

DNA:

Deoxyribonucleic acid

GSK-3β:

Glycogen synthase kinase-β

GRH:

Gonadotropin-releasing hormone

G-Px:

Glutathione peroxidase

4-HNE:

4-hydroxy-nonenal

HSP:

Heat shock protein

5-HTT:

Serotonin transporter

IL-1β:

Interleucine-1β

IFN-γ:

Interferon-γ

IL-1:

Interleukin-1

IL-6R:

Interleukin-6 receptor

JAK:

Janus kinase

JNK 1–3:

Jun NH2 kinases 1–3

MAPK:

Mitogen-activated protein kinase

MCI:

Mild cognitive impairment

MDD:

Major depressive disorder

NGF:

Nerve growth factor

NFT:

Neurofibrillary tangle

NMDA:

N-Methyl-dextro-aspartate

NMDAR:

NMDA receptor

NO:

Nitric oxide

NSAID:

Non-steroidal anti-inflammatory drugs

NSD:

Not senile dementia

PET:

Positron emission tomography

PKC:

Protein kinase C

RNS:

Reactive nitrogen species

ROS:

Reactive oxygen species

SDAT:

Senile dementia of Alzheimer type

SP:

Senile plaque

Tau:

Tau protein

TNF-ɑ:

Tumor necrosis factor-ɑ

TRK-β:

Tyrosine-receptor kinase-β

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Acknowledgments

George Perry is supported by the Semmes Foundation, Inc.; the Alzheimer Association; and by a grant from the National Institute on Minority Health and Health Disparities (G12MD007591) from the National Institutes of Health.

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The authors declare that they have no conflict of interest.

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Authors and Affiliations

  1. College of Sciences, The University of Texas at San Antonio, One UTSA Circle, San Antonio, TX, 78249, USA

    Roberto Rodrigues

  2. Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH, 44106-7288, USA

    Robert B. Petersen

  3. Department of Biology, The University of Texas at San Antonio,College of Sciences, One UTSA Circle, San Antonio, TX, 78249, USA

    George Perry

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Rodrigues, R., Petersen, R.B. & Perry, G. Parallels Between Major Depressive Disorder and Alzheimer’s Disease: Role of Oxidative Stress and Genetic Vulnerability. Cell Mol Neurobiol 34, 925–949 (2014). https://doi.org/10.1007/s10571-014-0074-5

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