Patients with neurodegenerative diseases have cognitive, motor, and behavioral impairments that negatively impact their quality of life. They are characterized by increasing neuronal dysfunction accompanied by extracellular and intracellular accumulation of misfolded proteins such as amyloid-beta, tau, alpha-synuclein, SOD1, TDP43, and others. These are primarily due to abnormal protein dynamics caused by ubiquitin–proteosome–autophagy system deficiency, oxidative stress and free radical formation, mitochondrial dysfunction, impaired bioenergetics, neurotrophin dysfunction, 'neuroinflammatory' processes, and (secondary) disruptions of neuronal Golgi apparatus and axonal transport. Surprisingly, there are both overlapping and intraindividual differences across distinct phenotypes that contribute to programmed cell death in a long run over many years.
While the "physiological" aging process, which includes a reduction in motor and cognitive abilities, has no substantial impact on daily tasks and activities. The most prevalent phenotypic presentations of neurodegeneration, on the other hand, are motor and cognitive impairment. Both signs commonly occur in the same disease, making "pure" motor or cognitive diseases difficult to distinguish. Movement abnormalities are frequently accompanied by cognitive problems, and movement difficulties are common in neurodegenerative dementias. Such phenotypic overlaps suggest approaching these conditions by highlighting the commonalities of entities traditionally considered distinct. There is currently a great need for knowledge concerning the management of old-age neurodegenerative diseases demonstrating clinical overlap between motor and cognitive features in neurodegeneration, including but not limited to Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis, Huntington’s disease, Dementia with Lewy bodies, Frontotemporal dementias, Multiple system atrophy, Progressive supranuclear palsy, Corticobasal degeneration, and Essential tremor. In this regard, common molecular etiologies including clinical and pathophysiological features of neurodegeneration must be re-examined in cellular, animal models, and humans, with a focus on motricity throughout the neurodegenerative spectrum.
The aim of this research topic is to discuss the molecular dynamics of cognitive-motor impairment in neurodegenerative diseases for developing disease-modifying therapy. We welcome the submission of Original Research, Meta-analysis, Review, Mini Review, Perspective, and Opinion Articles that address but are not limited to:
1. Motor and cognitive features characterizing “physiological” aging processes.
2. Neurodegeneration guided pathological aging with cognitive and motor abnormalities.
3. Neuroplasticity at cortical synapses in people with dementia and movement disorders.
4. Synergistic mechanisms between pathogenic proteins in neurodegeneration.
5. Molecular crosstalk between overlapping neurodegenerative disease phenotypes.
Patients with neurodegenerative diseases have cognitive, motor, and behavioral impairments that negatively impact their quality of life. They are characterized by increasing neuronal dysfunction accompanied by extracellular and intracellular accumulation of misfolded proteins such as amyloid-beta, tau, alpha-synuclein, SOD1, TDP43, and others. These are primarily due to abnormal protein dynamics caused by ubiquitin–proteosome–autophagy system deficiency, oxidative stress and free radical formation, mitochondrial dysfunction, impaired bioenergetics, neurotrophin dysfunction, 'neuroinflammatory' processes, and (secondary) disruptions of neuronal Golgi apparatus and axonal transport. Surprisingly, there are both overlapping and intraindividual differences across distinct phenotypes that contribute to programmed cell death in a long run over many years.
While the "physiological" aging process, which includes a reduction in motor and cognitive abilities, has no substantial impact on daily tasks and activities. The most prevalent phenotypic presentations of neurodegeneration, on the other hand, are motor and cognitive impairment. Both signs commonly occur in the same disease, making "pure" motor or cognitive diseases difficult to distinguish. Movement abnormalities are frequently accompanied by cognitive problems, and movement difficulties are common in neurodegenerative dementias. Such phenotypic overlaps suggest approaching these conditions by highlighting the commonalities of entities traditionally considered distinct. There is currently a great need for knowledge concerning the management of old-age neurodegenerative diseases demonstrating clinical overlap between motor and cognitive features in neurodegeneration, including but not limited to Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis, Huntington’s disease, Dementia with Lewy bodies, Frontotemporal dementias, Multiple system atrophy, Progressive supranuclear palsy, Corticobasal degeneration, and Essential tremor. In this regard, common molecular etiologies including clinical and pathophysiological features of neurodegeneration must be re-examined in cellular, animal models, and humans, with a focus on motricity throughout the neurodegenerative spectrum.
The aim of this research topic is to discuss the molecular dynamics of cognitive-motor impairment in neurodegenerative diseases for developing disease-modifying therapy. We welcome the submission of Original Research, Meta-analysis, Review, Mini Review, Perspective, and Opinion Articles that address but are not limited to:
1. Motor and cognitive features characterizing “physiological” aging processes.
2. Neurodegeneration guided pathological aging with cognitive and motor abnormalities.
3. Neuroplasticity at cortical synapses in people with dementia and movement disorders.
4. Synergistic mechanisms between pathogenic proteins in neurodegeneration.
5. Molecular crosstalk between overlapping neurodegenerative disease phenotypes.
