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Psychosocial Aspects of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The pathophysiology of PTSD is not completely understood. The size of the hippocampus is inversely related to PTSD and the success of its treatment. The smaller the hippocampus, the higher the risk of PTSD. During trauma, higher levels of stress hormones suppress the activities of the hypothalamus. This may be a major factor in the development of PTSD. There are also low levels of serotonin, contributing to anxiety, aggression, irritability, impulsivity, an inability to stop thinking about traumatic events, and even suicidal thoughts. Low levels of dopamine promote anhedonia, apathy, impaired attention, and motor deficits. High levels of dopamine promote motor deficits, restlessness, psychosis, and agitation. There is less-than-normal activity in the dorsal and rostral anterior cingulate cortices and ventromedial prefrontal cortex. These areas are linked to experiencing and regulating of emotions. The pathophysiological relationship between PTSD and diabetes mellitus is not fully understood. However, a sustained activation of the hormonal stress axis, because of chronic stress symptoms, is likely implicated.
Exocytosis of Nonclassical Neurotransmitters
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Xiao Su, Vincent R. Mirabella, Kenneth G. Paradiso, Zhiping P. Pang
Dopamine plays important functions including motor control, decision making, and reward. The most well-studied dopamine-secreting neurons are located in the substantia nigra pars compacta (SNpc) and the ventral tegmental area (VTA) in midbrain region and project to the striatum to regulate essential functions including movement, motivation, and reward-mediated learning (Howe and Dombeck, 2016).
Organic Nanocarriers for Brain Drug Delivery
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Marlene Lúcio, Carla M. Lopes, Eduarda Fernandes, Hugo Gonẹalves, Maria Elisabete C. D. Real Oliveira
PD is also a neurodegenerative disease with several aetiologies, including the death of dopamine-generating neurons in the brain area called substantia nigra, which causes a decrease in dopamine levels and motor symptoms such as tremor and rigidity. Currently available therapies are based on the administration of a natural precursor of dopamine (levodopa). In this regard, liposomal formulations composed by PC and Chol and loaded with levodopa were i.p. administered in mice, improving the release of dopamine in the striatum region [95, 96]. Moreover, these formulations by carrying levodopa to the brain avoided peripheral conversion to dopamine, which causes side effects of nausea, sleepiness and dyskinesia (involuntary movements which may occur with long-term levodopa use). Levodopa-loaded liposomes have also inhibited akinaesia (a failure to move or a much smaller version of movement) more effectively.
Mood disorders and hormonal status across women’s life: a narrative review
Published in Gynecological Endocrinology, 2022
Alice Antonelli, Andrea Giannini, Peter Chedraui, Patrizia Monteleone, Marta Caretto, Alessandro D. Genazzani, Paolo Mannella, Tommaso Simoncini, Andrea R. Genazzani
Dopamine is a neurotransmitter present at a central level in the striatum, substantia nigra and hypothalamus and involved not only in motor control but also in learning and motivation. Estrogen and progesterone can modulate its activity by acting both through the regulation of its synthesis, release, turnover and by modifying the response and density of its receptors [41]. Estrogen mainly has a stimulating action on dopaminergic neurotransmission while progesterone appears effective only when preceded by estrogen treatment [42]. Some researchers have focused on the expression of catechol-o-methyltransferase (COMT) during the various phases of the menstrual cycle, showing a different enzymatic activity: high COMT activity before ovulation associated with low levels of dopamine and high levels of estrogen and low COMT activity during menstruation with high dopamine plasma concentrations and low estrogen levels [43]. This sets the stage for devising adequate hormone therapy in patients with mood dopamine dependent disorders, although further investigations are needed.
l -Theanine ameliorates motor deficit, mitochondrial dysfunction, and neurodegeneration against chronic tramadol induced rats model of Parkinson’s disease
Published in Drug and Chemical Toxicology, 2022
Khadga Raj, G. D. Gupta, Shamsher Singh
Additionally, long-term toxin exposure and excessive use of opioid drugs like tramadol enhance oxidative stress, alter neurotransmitters level, and damage to dopaminergic neurons. Reduced neutralization and overproduction of ROS can lead to mitochondrial damage, including mutations in mitochondrial DNA, affect to the mitochondrial respiratory chain, permeability, and disruption to Ca2+ homeostasis. Therefore, mitochondrial damage plays an important role in the pathogenesis of neurodegenerative diseases including PD (Guo et al.2013). The available treatments of PD only increase the dopamine level in the striatum to restore the associated motor deficits. These includes dopamine precursor (levodopa), agonists of dopamine (ropinirole, pramipexole, lisuride, and rotigotine), MAO-B inhibitors (rasagiline and selegiline). However, these approaches do not provide long-term neuroprotection (Velázquez-Paniagua et al.2016). Similarly, long-term use of dopamine precursor is reported to initiate abnormal movements such as dyskinesia, known as l-DOPA induced dyskinesia (LID) and reduces motor ability in PD (Cenci 2014). Presently, available drugs provide symptomatic benefits without reversion or slowing of disease pathogenesis. Hence, there is a need to find out potential drug molecules or target sites that can overcome PD (Oertel 2017).
Drug treatment strategies for depression in Parkinson disease
Published in Expert Opinion on Pharmacotherapy, 2019
Melody Ryan, Courtney V. Eatmon, John T. Slevin
Dopamine is involved in motor, cognitive, and emotional and motivational pathways in the brain. The decrease in dopamine in the basal ganglia affects motor function through interaction with the globus pallidum interna, thalamus, and cerebral cortex and leads to the common motor symptoms of PD. The dysfunction of the cognitive pathways may be responsible for the dementia often seen in later PD. The emotional and motivational pathway problems may, in part, account for the depressive symptoms that predate motor dysfunction in PD. Early in PD, dopaminergic neurons in the substania nigra pars compacta degenerate. In turn, there is less stimulation of the ventral striatum which is involved in the reward and motivation [48]. Nuclear medicine studies have shown a decrease in dopamine in the caudate nucleus and the putamenal areas of the striatum in patients with PD and depression compared to non-depressed patients with PD [49]. The thalamus contains less dopamine in PD, not only does this affect motor function, but, because of the connectivity between the thalamus and the amygdala, it also affects emotions [38].