Identification of 22q11.2 deletion in a patient with schizophrenia and clinically diagnosed Rubinstein-Taybi syndrome.

Background: Rubinstein-Taybi syndrome (RTS) is a rare autosomal-dominant disease. Almost all cases are sporadic and attributed to de novo variant. Psychotic symptoms in RTS are rare and have been reported in only a few published cases.

Serum levels and mutual correlations of amyloid β in patients with depression.

Aim: Epidemiological studies have shown that depression is a risk factor for Alzheimer's disease (AD). Although the biological mechanism underlying the link between depression and AD is unclear, altered amyloid β (Aβ) metabolism in patients with depression has been suggested as a potential mechanism. Results from previous studies of Aβ metabolism in patients with depression have been inconsistent, and Aβ polymerization, which is a crucial process in AD pathology, has not previously been assessed.

Serum levels of TDP-43 in late-life patients with depressive episode.

Background: Recent reports have suggested a relationship between affective disorder including depression and bipolar disorder (BP) and frontotemporal dementia (FTD). TAR DNA binding protein (TDP) -43 is a protein found in the brain and peripheral fluid of patients with FTD. To examine a possible association between affective disorders and FTD, serum levels of TDP-43 were evaluated in late-life patients with major depressive episode (MDE).

Increased Serum Levels of α-Synuclein in Patients With Major Depressive Disorder.

Objective: Epidemiologic studies have demonstrated that depression is a risk factor for dementia. In particular, dementia with Lewy bodies (DLB) has been noted to be highly relevant to depression. It has been suggested that α-synuclein (α-syn), a major component of Lewy bodies, is related to the onset and progression of DLB.

Glucocorticoid may influence amyloid β metabolism in patients with depression.

Epidemiological studies have demonstrated that depression may be a risk factor for Alzheimer's disease (AD); however, the biological mechanisms of the transition from depression to AD are still not clear. Changes of amyloid β protein (Aβ) metabolism and increased glucocorticoid (GC) levels have been found in both depression and AD. Moreover, several studies in animal models have demonstrated that GC administration changes Aβ metabolism.

Residual memory impairment in remitted depression may be a predictive factor for recurrence.

Objective: Memory impairment in remitted depression is reported to be related to the number of previous depressive episodes. A recent report hypothesized that each depressive episode increases the risk of memory impairment during remission, which further increases the risk of recurrence. We investigated whether the risk for recurrence increased as a function of memory impairment at remission.

Psychomotor agitation in major depressive disorder is a predictive factor of mood-switching.

Background: The relationship between psychomotor agitation in unipolar depression and mood-switching from depression to manic, hypomanic and mixed states has been controversial. We investigated the future risk of initial mood-switching as a function of psychomotor agitation in unipolar depression.

Methods: We identified 189 participants diagnosed with major depressive disorder (MDD).

Gender differences in serum testosterone and cortisol in patients with major depressive disorder compared with controls.

Objective: Testosterone may have a role distinct from cortisol in the pathophysiology of depression. The hypothalamus-pituitary-adrenal (HPA) axis affects the functions of sex steroid hormones through interaction with corticotropin-releasing hormone (CRH) and gonadotropin-releasing hormone (GnRH). The objective of this study was to investigate differences in serum levels of testosterone and cortisol in male and female patients with major depressive disorder (MDD).

Serum dehydroepiandrosterone (DHEA) and DHEA-sulfate (S) levels in medicated patients with major depressive disorder compared with controls.

Background: There is accumulating evidence regarding gender differences in clinical symptoms or response to antidepressants in patients with depression. However, less attention has been given to sex differences in the underlying biological mechanisms of depression. The adrenal androgens, dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEA-S), play a critical role in controlling affect, mood, and anxiety.