Neural plasticity
-
Many studies in human and animal models have shown that neural plasticity compensates for the loss of motor function after stroke. However, neural plasticity concerning compensatory movement, activated ipsilateral motor projections and competitive interaction after stroke contributes to maladaptive plasticity, which negatively affects motor recovery. Compensatory movement on the less-affected side helps to perform self-sustaining activity but also creates an inappropriate movement pattern and ultimately limits the normal motor pattern. ⋯ To minimize this maladaptive plasticity, rehabilitation programs should be selected according to the motor impairment of stroke patients. Noninvasive brain stimulation might also be useful for correcting maladaptive plasticity after stroke. Here, we review the underlying mechanisms of maladaptive plasticity after stroke and propose rehabilitation approaches for appropriate cortical reorganization.
-
Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease principally affecting motor neurons. Besides motor symptoms, a subset of patients develop cognitive disturbances or even frontotemporal dementia (FTD), indicating that ALS may also involve extramotor brain regions. ⋯ Particularly, neuropathological findings suggest that ALS not only affects the frontotemporal network but rather is part of a wide clinicopathological spectrum of brain disorders known as TAR-DNA binding protein 43 (TDP-43) proteinopathies. This paper reviews the current state of knowledge concerning the neuropsychological and neuropathological sequelae of TDP-43 proteinopathies, with special focus on the neuroimaging findings associated with cognitive change in ALS.
-
The pathological hallmarks of Alzheimer's disease (AD)--widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles--have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. Transgenic mice have been developed based on rare familial forms of AD and frontotemporal dementia, allowing investigators to test in detail the structural, functional, and behavioral consequences of AD-associated pathology. ⋯ These changes in synapse structure and function as well as frank synapse and neuronal loss contribute to the neural system dysfunction which causes cognitive deficits. Understanding the underpinnings of dementia in AD will be essential to develop and evaluate therapeutic approaches for this widespread and devastating disease.