GROWTH FACTORS DECREASE IN SUBJECTS WITH MILD TO MODERATE ALZHEIMER'S DISEASE (AD): POTENTIAL CORRECTION WITH DEHYDROEPIANDROSTERONE-SULPHATE (DHEAS)
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Neurobiological links between depression and AD: The role of TGF-β1 signaling as a new pharmacological target
2018, Pharmacological ResearchCitation Excerpt :Intranasal administration of TGF-β1, before i.c.v. Aβ(1-42) injection, prevented Aβ-induced increases in microglia-derived proinflammatory mediators (TNF-α, IL-1β and iNOS), thereby preventing amyloid-related neurodegeneration [118]. Coming back to MCI and AD patients, several studies have found a significant decrease in the plasma levels of the active (25 kDa) and inactive (50 kDa) forms of TGF-β1 in AD patients [140–142], as well as a reduced secretion of TGF-β1 from circulating peripheral blood mononuclear cells [143]. Interestingly, the deficit of TGF-β1 has been detected in the early phase of AD (preclinical AD) and, in particular, in amnestic MCI patients [144].
Steroid sulfatase inhibitor DU-14 protects spatial memory and synaptic plasticity from disruption by amyloid β protein in male rats
2016, Hormones and BehaviorCitation Excerpt :The mechanistic pathway that underlying the behavioral and electrophysiological effects of DU-14 is closely associated with the increased DHEAS. According to previous studies, up-regulation of DHEAS in the brain could: 1) block Aβ1–42 induced intracellular calcium overload (Kato-Negishi and Kawahara, 2008); 2) increase the production of growth factors (Luppi et al., 2009) and enhance brain cholinergic function (Dong and Zheng, 2012); 3) play an immunomodulatory role on NK functional activity in physiological aging and AD (Solerte et al., 1999); 4) have an antiglucocorticoid activity and neuroprotective effects, while its levels decreased in AD (Murialdo et al., 2001); 5) prevent the cells from entering late apoptosis and necrosis and stimulate neurite outgrowth per se (El Bitar et al., 2014); 6) protect hippocampal neurons against glutamate through elevating a kappaB-dependent transcription factor activity (Leskiewicz et al., 2008; Mao and Barger, 1998). Of course, a further investigation on the effects of DU-14 and its mechanisms in AD transgenic animals or AD patients would be urgently required in the future.
DHEA and cognitive function in the elderly
2015, Journal of Steroid Biochemistry and Molecular BiologyDaily stressors and adult day service use by family caregivers: Effects on depressive symptoms, positive mood, and dehydroepiandrosterone-sulfate
2014, American Journal of Geriatric PsychiatryCitation Excerpt :In turn, low levels of DHEA-S among older people have been linked to cancer, insulin resistance, cardiovascular disease, and immune system deficiencies.9,21 Although acute stress typically leads to increases in DHEA-S, prolonged exposure to stressors attenuates DHEA-S levels, thereby reducing its health protective effects.8,20 DHEA-S levels also decrease with age.10
VEGF plasma level variations in duloxetine-treated patients with major depression
2013, Journal of Affective DisordersCitation Excerpt :There is strong association between depression (or other CNS pathologies such as Alzheimer's disease) and cardiovascular disease, suggesting a possible role of neurovascular unit abnormalities, possibly characterized by endothelial degenerations, capillary density changes and neuroinflammation (Fioravanzo et al., 2010; Taylor et al., 2013; Warner-Schmidt and Duman, 2008). A decrease in VEGF levels was observed in Alzheimer's disease, schizophrenia and autism (Emanuele et al., 2010; Fulzele and Pillai, 2009; Luppi et al., 2009), while an increase in VEGF levels was detected during acute manic episodes, in occurrences of prolonged psychosocial stress and anxiety conditions (Asberg et al., 2009; Kwon et al., 2011; Lee and Kim, 2012). A number of treatments have been shown to affect VEGF signaling.