Accumulation of misfolded protein in neurons is a common feature of many neurodegenerative diseases.
Sequential activation of neurons is a common feature of network activity during a variety of behaviors, including working memory and decision making.
Background and Objectives: Neuropathic pain following injury to peripheral sensory neurons is a common clinical problem and frequently difficult to treat.
Transient bursting behaviour of excitable cells, such as neurons, is a common feature observed experimentally, but theoretically, it is not well understood.
Selective vulnerability of specific subsets of neurons is a common feature of neurodegenerative diseases [43].
This class of neurons is a common feature of tectal cytoarchitectural organization in vertebrates, with galeomorph sharks, skates and rays being the exception to the rule.
ALS is often considered a proteinopathy because the generation of misfolded or abnormal proteins with the propensity to aggregate and accumulate in damaged neurons is a common feature of both sporadic ALS (sALS) and familial ALS (fALS) [ 6, 20].
While peripheral sensory neurotoxicity mediated by DNA-cross links with positive charged molecules formed by hydrolytic aquation in dorsal root ganglion neurons is a common side effect of platinum-based antineoplastic drugs affecting almost one in two treated patients, cytotoxic effects of cisplatin to the central nervous system are not well elucidated [ 16, 17].
However, in subjects with autism of unknown etiology, smaller neurons were a common finding in the claustrum and magnocellular basal complex.
On the other hand, cerebral microcirculatory disturbances, together with other neurotoxicity mediators such as Na+, Ca2+ and Glu, are detrimental to neuronal survival in the ischemic penumbra or peri-infarct zone; apoptotic neuron death is a common outcome.
