Prevalence and Incidence of Major Depressive Disorder in Alzheimer’s Disease: Findings from Two Databases

2001 ◽  
Vol 13 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Myron F. Weiner ◽  
Rachelle S. Doody ◽  
Ramesh Sairam ◽  
Barbara Foster ◽  
Tso-yu Liao
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Major Depressive

scholarly journals Neurobiological substrates underlying the effect of genomic risk for depression on the conversion of amnestic mild cognitive impairment

Brain ◽  
2018 ◽  
Vol 141 (12) ◽  
pp. 3457-3471 ◽  
Author(s):  
Jiayuan Xu ◽  
Qiaojun Li ◽  
Wen Qin ◽  
Mulin Jun Li ◽  
Chuanjun Zhuo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Major Depressive Disorder ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Depressive Disorder ◽  
Genetic Variants ◽  
Amnestic Mild Cognitive Impairment ◽  
Risk Scores ◽  
Major Depressive

Abstract Depression increases the conversion risk from amnestic mild cognitive impairment to Alzheimer’s disease with unknown mechanisms. We hypothesize that the cumulative genomic risk for major depressive disorder may be a candidate cause for the increased conversion risk. Here, we aimed to investigate the predictive effect of the polygenic risk scores of major depressive disorder-specific genetic variants (PRSsMDD) on the conversion from non-depressed amnestic mild cognitive impairment to Alzheimer’s disease, and its underlying neurobiological mechanisms. The PRSsMDD could predict the conversion from amnestic mild cognitive impairment to Alzheimer’s disease, and amnestic mild cognitive impairment patients with high risk scores showed 16.25% higher conversion rate than those with low risk. The PRSsMDD was correlated with the left hippocampal volume, which was found to mediate the predictive effect of the PRSsMDD on the conversion of amnestic mild cognitive impairment. The major depressive disorder-specific genetic variants were mapped into genes using different strategies, and then enrichment analyses and protein–protein interaction network analysis revealed that these genes were involved in developmental process and amyloid-beta binding. They showed temporal-specific expression in the hippocampus in middle and late foetal developmental periods. Cell type-specific expression analysis of these genes demonstrated significant over-representation in the pyramidal neurons and interneurons in the hippocampus. These cross-scale neurobiological analyses and functional annotations indicate that major depressive disorder-specific genetic variants may increase the conversion from amnestic mild cognitive impairment to Alzheimer’s disease by modulating the early hippocampal development and amyloid-beta binding. The PRSsMDD could be used as a complementary measure to select patients with amnestic mild cognitive impairment with high conversion risk to Alzheimer’s disease.

scholarly journals Associations between gut microbiota and Alzheimer’s disease, major depressive disorder, and schizophrenia

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Zhenhuang Zhuang ◽  
Ruotong Yang ◽  
Wenxiu Wang ◽  
Lu Qi ◽  
Tao Huang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Major Depressive Disorder ◽  
Gut Microbiota ◽  
Depressive Disorder ◽  
Lower Risk ◽  
Neuropsychiatric Disorders ◽  
Microbiota Composition ◽  
Major Depressive ◽  
Gut Microbiota Composition

Abstract Background Growing evidence has shown that alterations in the gut microbiota composition were associated with a variety of neuropsychiatric conditions. However, whether such associations reflect causality remains unknown. We aimed to reveal the causal relationships among gut microbiota, metabolites, and neuropsychiatric disorders including Alzheimer’s disease (AD), major depressive disorder (MDD), and schizophrenia (SCZ). Methods A two-sample bi-directional Mendelian randomization analysis was performed by using genetic variants from genome-wide association studies as instrumental variables for gut microbiota, metabolites, AD, MDD, and SCZ, respectively. Results We found suggestive associations of host-genetic-driven increase in Blautia (OR, 0.88; 95%CI, 0.79–0.99; P = 0.028) and elevated γ-aminobutyric acid (GABA) (0.96; 0.92–1.00; P = 0.034), a downstream product of Blautia-dependent arginine metabolism, with a lower risk of AD. Genetically increased Enterobacteriaceae family and Enterobacteriales order were potentially associated with a higher risk of SCZ (1.09; 1.00–1.18; P = 0.048), while Gammaproteobacteria class (0.90; 0.83–0.98; P = 0.011) was related to a lower risk for SCZ. Gut production of serotonin was potentially associated with an increased risk of SCZ (1.07; 1.00–1.15; P = 0.047). Furthermore, genetically increased Bacilli class was related to a higher risk of MDD (1.07; 1.02–1.12; P = 0.010). In the other direction, neuropsychiatric disorders altered gut microbiota composition. Conclusions These data for the first time provide evidence of potential causal links between gut microbiome and AD, MDD, and SCZ. GABA and serotonin may play an important role in gut microbiota-host crosstalk in AD and SCZ, respectively. Further investigations in understanding the underlying mechanisms of associations between gut microbiota and AD, MDD, and SCZ are required.

Reduced plasma oestrogen stimulated neurophysin and delayed response to oestrogen challenge in Alzheimer's disease

1990 ◽  
Vol 20 (4) ◽  
pp. 773-777 ◽  
Author(s):  
Janice Christie ◽  
Robert Hunter ◽  
John Bennie ◽  
Helen Wilson ◽  
Sheena Carroll ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Plasma Concentrations ◽  
Delayed Response ◽  
Major Depressive

SynopsisPlasma concentrations of oestrogen stimulated neurophysin (ESN) were reduced in 28 patients with Alzheimer's disease (AD) compared with 14 age-matched controls, 16 patients with other presenile dementias and 12 patients with major depressive disorder. The ESN response to oestrogen challenge was delayed in 10 AD patients compared with 7 age-matched controls. Reduced basal and oestrogen stimulated plasma ESN may be related to impaired responsiveness of the hypothalamo-neurohypophysial neurons and/or a reduction in the amount of pituitary ESN available for release. Plasma ESN measurements may be of value for excluding the diagnosis of AD in patients with dementia who present before the age of 65.

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