Neurological processes behind depression in individuals with dementia
The swelling of the brain tissue that takes place when a patient is depressed might cause the onset of dementia (Rief et al 2016) Specific proteins situated in the brain that multiply with depression may also increase the possibility of dementia. The other way to look at it is to consider brain shrinkage that is as a result of excessive amounts of specific stress hormones (Fletcher et al 2013). Alternatively, the gradual development of dementia may be caused by metabolic factors, brain tumors, or subdural hematomas. It is, therefore, safe to say that persistent depression and stress are the start points of abnormal production of corticosteroids which, on the other hand, cause rapture to the hippocampus. The resulting injury may not be exact but leads to cognitive and neuronal reservoirs.
SSRIs have different structures, but have similar modes of action, by inhibiting the serotonin transporter (Hirsch & Birnbaum 2016). Depression begins with the onset of reduced levels of 5-HT in the brain. The SSRIs are known to refurbish the concentration of 5-HT in the synaptic cloven. Such a process is achieved by attaching at the 5-HT re-uptake transporter inhibiting the absorption and the following 5-HT breakdown. The re-uptake inhibition leads to the building-up of 5-HT in the synaptic left and the volume of 5-HT returns within the required levels. Antipsychotic drugs are classified as either atypical or typical (Mauri et al 2014). The achievement of a practical antipsychotic effect is attained in atypical when its prototype is already at 45% D2 receptor occupancy. For typical antipsychotic drugs, a sufficient impact is reached at 70% blockade.
The mechanism of action of antipsychotics varies slightly depending on the type described above. For typical antipsychotics, it involves the D2 receptor blockade of postsynaptic in the mesolimbic pathway. The most common are anticholinergic effects, which include constipation, blurred vision, urinary retention, cognitive impairment, and dry mouth. The symptoms mentioned can lead to, gastrointestinal obstruction, falls, or tooth decay. Low-cogency clozapine and FGAs are major risk factors for anticholinergic effects (ÜÇOk, A. L. P. An extra electrocardiogram is necessary if the methadone prescription is over 100mg/d or if patients display seizures. If the QTc interval exceeds 450 ms but within 500 ms, review the inherent benefits and risks with patients and observe them regularly. If the QTc interval is greater than 500 ms, consider reducing or discounting the methadone dose, or using an alternative therapy.
Education on the choice of therapy and the balancing of risks and benefits associated with the use of antipsychotics and antidepressants. Depression and other mental disorders are debilitating and complex at the same time. Alternatively, the doctor can explore the possibility of the periodic use of these drugs. The method works in the way that the drugs are prescribed during times of crisis, and their usage gradually reduced as the patient improves (Wang et al 2011). Though, it is critical to note that there is there is no guarantee that the drugs themselves will not aggravate the problems and appear to necessitate their long-term use. Most importantly, educating the patients and their families about the benefits and risks, all the steps involved in medication, and the side effects of therapy are necessary.
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