Depression Treatment: Bright Light Therapy in Parkinson’s Disease: An Overview of the Background and Evidence.

Bright light therapy in Parkinson’s disease: an overview of the background and evidence.

Filed under: Depression Treatment

Parkinsons Dis. 2012; 2012: 767105
Rutten S, Vriend C, van den Heuvel OA, Smit JH, Berendse HW, van der Werf YD

Sleep disorders are common in Parkinson’s disease (PD) and seem to be strongly associated with depression. It has been suggested that sleep disorders as well as depression are caused by a disturbed circadian rhythm. Indeed, PD patients are prone to misalignment of their circadian rhythm due to various factors, and many patients with PD display a phase advance of their circadian rhythm. Current treatment options for sleep disorders and depression in patients with PD are limited and can have serious side effects; alternative treatments are therefore badly needed. Bright light therapy (BLT) restores circadian rhythmicity effectively in mood- and sleep-disturbed patients without PD. The few studies that focused on the efficacy of BLT in patients with PD demonstrated a positive effect of BLT not only on sleep and mood but also on motor function. More research on the neurobiology and efficacy of BLT in PD is warranted.
HubMed – depression

Roles of PI3K/AKT/GSK3/mTOR Pathway in Cell Signaling of Mental Illnesses.

Filed under: Depression Treatment

Depress Res Treat. 2012; 2012: 752563
Kitagishi Y, Kobayashi M, Kikuta K, Matsuda S

Several pharmacological agents acting on monoamine neurotransmission are used for the management of mental illnesses. Regulation of PI3K/AKT and GSK3 pathways may constitute an important signaling center in the subcellular integration of the synaptic neurotransmission. The pathways also modulate neuronal cell proliferation, migration, and plasticity. There are evidences to suggest that inflammation of neuron contributes to the pathology of depression. Inflammatory activation of neuron contributes to the loss of glial elements, which are consistent with pathological findings characterizing the depression. A mechanism of anti-inflammatory reactions from antidepressant medications has been found to be associated with an enhancement of heme oxygenase-1 expression. This induction in brain is also important in neuroprotection and neuroplasticity. As enzymes involved in cell survival and neuroplasticity are relevant to neurotrophic factor dysregulation, the PI3K/AKT/GSK3 may provide an important signaling for the neuroprotection in depression. In this paper, we summarize advances on the involvement of the PI3K/AKT/GSK3 pathways in cell signaling of neuronal cells in mental illnesses.
HubMed – depression

Serotonergic modulation of Neural activities in the entorhinal cortex.

Filed under: Depression Treatment

Int J Physiol Pathophysiol Pharmacol. 2012; 4(4): 201-10
Lei S

The entorhinal cortex (EC) is considered as the gate to control the flow of information into and out of the hippocampus. The EC is important for numerous physiological functions such as emotional control, learning and memory and pathological disorders including Alzheimer’s disease, schizophrenia and temporal lobe epilepsy. Serotonin is a classical neurotransmitter which may modify these physiological functions and pathology of neurological diseases. The EC receives profuse serotonergic innervations from the raphe nuclei in the brainstem and expresses high density of serotonergic receptors including 5-HT(1A), 5-HT(1D), 5-HT(1E), 5-HT(2A), 5-HT(3) and 5-HT(6). The prominent innervation by serotonergic neurons and the dense expression of serotonergic receptors in the EC suggest that serotonin is a major modulator in this brain region. Serotonin exerts inhibitory effects in the EC. Serotonin hyperpolarizes entorhinal neurons and inhibits the excitatory synaptic transmission via activation of 5-HT(1A) receptors but facilitates GABA release via activation of 5-HT(2A) receptors. Both 5-HT(1A) and 5-HT(2A) receptors are required for serotonin-induced inhibition of epileptiform activity although 5-HT(3) receptors may be involved in serotonin-mediated inhibition of acetylcholine release in the EC. Furthermore, the functions of serotonin in the EC may be implicated in Parkinson’s disease, Alzheimer’s disease and depression. Thus, understanding the roles of serotonergic modulation in the EC is of major clinical importance. Here, I review recent findings concerning the effects of serotonin on neural circuitry activity in the EC.
HubMed – depression

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