1,721,080 research outputs found
Alzheimer’s disease: from molecular pathogenesis to innovative therapies
Alzheimer’s disease is the most common neurodegenerative disorder and most prevalent cause of dementia in the elderly. Current standard treatment of Alzheimer’s disease is based on the use of acetylcholinesterase inhibitors, which have shown symptomatic benefits on cognitive, functional and behavioral symptoms of the disease. A growing body of evidence suggests that the accumulation of amyloid β-peptides may play a pivotal role in the pathogenesis of Alzheimer’s disease (amyloid hypothesis). The incremental progress in elucidating the molecular basis of Alzheimer’s disease is pointing the way towards more targeted and pathogenically specific treatment approaches. This review analyzes the available data on the new directions of Alzheimer’s disease therapy, with particular focus on secretase inhibitors, amyloid β-peptide vaccination,anti-inflammatory agents, metal chelators and cholesterol-lowering drugs
Process for reducing neuromuscular fatigue caused by exercise
A process for reducing neuromuscular fatigue caused by exercise comprises applying an anodal trans-cranial direct current stimulation over the right motor cortex of a person
Pathophysiology of spasticity
Spasticity arises from lesions involving the corticoreticulospinal system in the brain, brainstem or spinal cord. Abnormal suprasegmental influences lead to increased spinal cord excitability and to impairment of interneuronal systems thereby giving rise to increased muscle tone, enhanced stretch reflexes, muscle overactivity and antagonist muscle co-contraction. Additionally, muscle paresis and immobilisation in a shortened position result over time in structural changes that involve muscles, joint, tendons and bones and contribute to muscle stiffness. Spasticity is a complex motor disorder that arises from a central nervous system dysfunction and causes changes at all locomotor system levels, from the cerebral cortex to muscles, joints and bone
Novel nonpharmacologic perspectives for the treatment of task-specific focal hand dystonia
Narrative Review: The pathophysiology of focal hand dystonia (FHD) has not yet been completely clarified. Although there is a loss of inhibition at multiple levels of the central nervous system, maladaptive plasticity of the cerebral cortex as well as impairments in sensory and motor representations have also been reported. All of these abnormalities can be viewed as an epiphenomenon of the primary-still unknown-abnormality underlying focal dystonia. The purpose of this review is to describe the underlying constructs of novel nonpharmacologic approaches for the treatment of FHD. Alternative or complementary approaches to botulinum toxin injections such as behavioral training strategies and brain stimulation techniques are reviewed. None of the proposed treatments appears to be definitive and applicable to all patients with FHD. Each treatment strategy elicited some benefit in a fraction of patients. The combination of more than one approach (retraining, immobilization, botulinum toxin, neuromodulation, etc.) could lead to a better control of FHD. J HAND THER. 2009;22:156-62
Evidence for minimal abnormalities of motor axonal excitability in restless leg syndrome
Razionale per la stimolazione cronica extra-durale della corteccia motoria nei disordini del movimento.
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