Aging is characterized by the decline and deterioration of functional cells and results in a wide variety of molecular damages and reduced physical and mental capacity. The knowledge on aging process is important because life expectancy is expected to rise until 2050. Aging cannot be considered a homogeneous process and includes different trajectories characterized by states of fitness, frailty, and disability. Frailty is a dynamic condition put between a normal functional state and disability, with reduced capacity to cope with stressors. This geriatric syndrome affects physical, neuropsychological, and social domains and is driven by emotional and spiritual components. Sarcopenia is considered one of the determinants and the biological substrates of physical frailty. Physical and cognitive frailty are separately approached during daily clinical practice. The concept of motoric cognitive syndrome has partially changed this scenario, opening interesting windows toward future approaches. Thus, the purpose of this manuscript is to provide an excursus on current clinical practice, enforced by aneddoctical cases. The analysis of the current state of the art seems to support the urgent need of comprehensive organizational model incorporating physical and cognitive spheres in the same umbrella.

The neurobiology of Parkinson’s disease and its progression has been investigated during the last few decades. Braak et al. proposed neuropathological stages of this disease based on the recognizable topographical extent of Lewy body lesions. This pathological process involves specific brain areas with an ascending course from the brain stem to the cortex. Post-mortem studies are of importance to better understand not only the progression of motor symptoms, but also the involvement of other domains, including cognition and behavior. The correlation between the neuropathological expansion of the disease and the clinical phases remains demanding. Neuroimaging, including magnetic resonance imaging (MRI), positron emission tomography (PET), and single photon emission computed tomography (SPECT), could help to bridge this existing gap by providing in vivo evidence of the extension of the disorders. In the last decade, we observed an overabundance of reports regarding the sensitivity of neuroimaging techniques. All these studies were aimed at improving the accuracy of Parkinson’s disease (PD) diagnosis and discriminating it from other causes of parkinsonism. In this review, we look at the recent literature concerning PD and address the new frontier of diagnostic accuracy in terms of identification of early stages of the disease and conventional neuroimaging techniques that, in vivo, are capable of photographing the basal ganglia network and its cerebral connections.

During aging, many physiological systems spontaneously change independent of the presence of chronic diseases. The reward system is not an exception and its dysfunction generally includes a reduction in dopamine and glutamate activities and the loss of neurons of the ventral tegmental area (VTA). These impairments are even more pronounced in older persons who have neurodegenerative diseases and/or are affected by cognitive and motoric frailty. All these changes may result in the occurrence of cognitive and motoric frailty and accelerated progression of neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases. In particular, the loss of neurons in VTA may determine an acceleration of depressive symptoms and cognitive and motor frailty trajectory, producing an increased risk of disability and mortality. Thus, we hypothesize the existence of a loop between reward system dysfunction, depression, and neurodegenerative diseases in older persons. Longitudinal studies are needed to evaluate the determinant role of the reward system in the onset of motoric-cognitive risk syndrome.

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The long-acting somatostatin analogue SMS 201-995 has been used efficaciously in the therapy of metastatic carcinoid tumor, vasoactive intestinal peptide producing islet cell carcinoma, acromegaly, and TSH secreting pituitary tumors. We report the development of a gallstone in a patient treated for 23 months with a long acting somatostatin analogue for a metastatic carcinoid tumor. Symptomatic improvement and a reduction in the urinary excretion of 5-hydroxyindoleacetic acid occurred. There was no evidence of a gallstone on ultrasound and CT scan of the abdomen prior to somatostatin therapy. A progressively enlarging, asymptomatic gallstone developed during therapy.