Lancet neurology
-
Multicenter Study Observational Study
Prediction of manifest Huntington's disease with clinical and imaging measures: a prospective observational study.
Although the association between cytosine-adenine-guanine (CAG) repeat length and age at onset of Huntington's disease is well known, improved prediction of onset would be advantageous for clinical trial design and prognostic counselling. We compared various measures for tracking progression and predicting conversion to manifest Huntington's disease. ⋯ US National Institutes of Health, US National Institute of Neurological Disorders and Stroke, and CHDI Foundation.
-
Spinal cord injury is currently incurable and treatment is limited to minimising secondary complications and maximising residual function by rehabilitation. Improved understanding of the pathophysiology of spinal cord injury and the factors that prevent nerve and tissue repair has fuelled a move towards more ambitious experimental treatments aimed at promoting neuroprotection, axonal regeneration, and neuroplasticity. ⋯ However, in view of recent advances in spinal cord injury research and demand from patients, clinicians, and the scientific community to push promising experimental treatments to the clinic, momentum and optimism exist for the translation of candidate experimental treatments to clinical spinal cord injury. The ability to rescue, reactivate, and rewire spinal systems to restore function after spinal cord injury might soon be within reach.
-
Elizabeth Bradbury is a Medical Research Council Senior Fellow at King's College London (London, UK). She trained as a neuroscientist at the Institute of Psychiatry and St Thomas' Hospital in London before becoming a group leader at King's in 2003. Her research focuses on understanding processes of injury and repair and developing therapies to restore function following CNS trauma, with a particular interest in glial scarring, extracellular matrix modification, and neuroplasticity after spinal cord injury.
-
Review
Neuroimaging in amyotrophic lateral sclerosis: insights into structural and functional changes.
In the past two decades, structural and functional neuroimaging findings have greatly modified longstanding notions regarding the pathophysiology of amyotrophic lateral sclerosis (ALS). Neuroimaging studies have shown that anatomical and functional lesions spread beyond precentral cortices and corticospinal tracts, to include the corpus callosum; frontal, sensory, and premotor cortices; thalamus; and midbrain. Both MRI and PET studies have shown early and diffuse loss of inhibitory cortical interneurons in the motor cortex (increased levels of functional connectivity and loss of GABAergic neurons, respectively) and diffuse gliosis in white-matter tracts. ⋯ A possible role of PET in the diagnosis of ALS has recently been proposed. However, most neuroimaging studies have pitfalls, such as a small number and poor clinical characterisation of patients, absence of adequate controls, and scarcity of longitudinal assessments. Studies involving international collaborations, standardised assessments, and large patient cohorts will overcome these shortcomings and provide further insight into the pathogenesis of ALS.