ABSTRACT
In the last decade, attention has become greater to the relationship between neurodegeneration and abnormal insulin signaling in the central nervous system, as insulin in the brain is implicated in neuronal survival, plasticity, oxidative stress and neuroinflammation. Diabetes mellitus and Parkinson's disease are both aging-associated diseases that are turning into epidemics worldwide. Diabetes mellitus and insulin resistance not only increase the possibility of developing Parkinson's disease but can also determine the prognosis and progression of Parkinsonian symptoms. Today, there are no available curative or disease modifying treatments for Parkinson's disease, but the role of insulin and antidiabetic medications in neurodegeneration opens a door to treatment repurposing to fight against Parkinson's disease, both in diabetic and nondiabetic Parkinsonian patients. Furthermore, it is essential to comprehend how a frequent and treatable disease such as diabetes can influence the progression of neurodegeneration in a challenging disease such as Parkinson's disease. Here, we review the present evidence on the connection between Parkinson's disease and diabetes and the consequential implications of the existing antidiabetic molecules in the severity and development of Parkinsonism, with a particular focus on glucagon-like peptide-1 receptor agonists.
ABSTRACT
Parkinson's disease and diabetes mellitus are two chronic disorders associated with aging that are becoming increasingly prevalent worldwide. Parkinson is a multifactorial progressive condition with no available disease modifying treatments at the moment. Over the last few years there is growing interest in the relationship between diabetes (and impaired insulin signaling) and neurodegenerative diseases, as well as the possible benefit of antidiabetic treatments as neuroprotectors, even in non-diabetic patients. Insulin regulates essential functions in the brain such as neuronal survival, autophagy of toxic proteins, synaptic plasticity, neurogenesis, oxidative stress and neuroinflammation. We review the existing epidemiological, experimental and clinical evidence that supports the interplay between insulin and neurodegeneration in Parkinson's disease, as well as the role of antidiabetic treatments in this disease.
Subject(s)
Diabetes Mellitus, Type 2 , Diabetes Mellitus , Parkinson Disease , Glucagon-Like Peptide-1 Receptor , Humans , Hypoglycemic Agents/pharmacology , Insulin , Parkinson Disease/drug therapyABSTRACT
Objetivo. La estimulación magnética transcraneal repetitiva podría ser útil como tratamiento no farmacológico para la espasticidad. El objetivo de este estudio es reevaluar el efecto clínico y los cambios neurofisiológicos que produce la estimulación theta-burst intermitente (ETBi) sobre la espasticidad de las extremidades inferiores en pacientes con esclerosis múltiple recurrente en un ensayo aleatorizado, doble ciego, controlado con placebo. Pacientes y métodos. Diecisiete pacientes en la fase remitente de la enfermedad fueron aleatoriamente asignados al grupo placebo o al grupo de tratamiento activo mediante estimulación magnética transcraneal repetitiva con protocolo ETBi sobre la corteza motora contralateral de la pierna más afectada. El procedimiento consistió en 10 sesiones diarias durante dos semanas. Cada sesión consistió en 10 ráfagas que contenían tres pulsos a 50 Hz repetidos a intervalos de 200 ms (5 Hz) cada 10 s para un total de 600 estímulos. El efecto de ETBi se evaluó mediante el uso de parámetros clínicos (como la escala de Ashworth modificada) y neurofisiológicos (ratio de amplitud H/M y duración del período cortical silente). Resultados. Dos semanas de ETBi sobre la corteza motora de la pierna más afectada no produjeron ningún efecto clínico significativo sobre la espasticidad en pacientes con esclerosis múltiple recurrente. Sin embargo, aunque de forma no significativa, se observó disminución de la ratio de amplitud H/M y un aumento de la duración del período cortical silente. Conclusión. El protocolo de estimulación utilizado en este estudio no parece tener un efecto terapéutico significativo. Sin embargo, recomendamos estudios adicionales, ya que los cambios neurofisiológicos fueron evidentes
Aim. It has been suggested that the repetitive transcranial magnetic stimulation could be useful as a non-pharmacological treatment for spasticity. The aim of this study was to evaluate the clinical and neurophysiological effects of high-frequency intermittent theta burst stimulation (iTBS) on lower limb spasticity in patients with relapsing multiple sclerosis in a randomized, double-blind placebo controlled trial. Patients and methods. Seventeen patients in the remitting phase of the disease were randomly allocated to sham or magnetic therapy group and underwent iTBS over contralateral motor cortex of the most affected leg once a day for two weeks. Each session consisted of 10 bursts containing three pulses at 50 Hz repeated at 200 ms intervals (5 Hz) every 10 s for a total of 600 stimuli. The iTBS effect was assessed by using clinical (such as the Modified Ashworth Scale) and neurophysiological (H/M amplitude ratio and cortical silent period duration) parameters. Results. Two-week iTBS over motor cortex of the most affected leg did not produce any significant clinical effect on spasticity. However, it decreases the H/M amplitude ratio and increases duration of cortical silent period but not significantly, in patients with relapsing multiple sclerosis. CONCLUSION. The stimulation protocol used in this study does not have significant therapeutic effect. Therefore, we do recommend further studies as neurophysiological changes were evident
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Transcranial Magnetic Stimulation , Multiple Sclerosis, Relapsing-Remitting/therapy , Muscle Spasticity/therapy , Double-Blind Method , Treatment OutcomeSubject(s)
Blindness, Cortical/chemically induced , Methanol/poisoning , Occipital Lobe/drug effects , Acidosis/chemically induced , Adult , Blindness, Cortical/diagnostic imaging , Combined Modality Therapy , Humans , Magnetic Resonance Imaging , Male , Necrosis , Neuroimaging , Occipital Lobe/diagnostic imaging , Occipital Lobe/pathology , Psychomotor Agitation/etiology , Tomography, X-Ray Computed , Visual Cortex/diagnostic imaging , Visual Cortex/drug effects , Visual Cortex/pathologyABSTRACT
No disponible
Subject(s)
Humans , Male , Adult , Blindness, Cortical/chemically induced , Blindness, Cortical/complications , Blindness, Cortical , Methanol/adverse effects , Methanol/toxicity , Depression/complications , Psychomotor Agitation/complications , Psychomotor Agitation/diagnosis , Tomography, Emission-Computed/instrumentation , Tomography, Emission-Computed/methods , Skull/pathology , Skull , Magnetic Resonance Imaging , Methanol/blood , Acidosis/metabolism , Hyperkalemia/complicationsABSTRACT
No disponible
