Sentence examples for neuron age from inspiring English sources

appear more related to the neuron age than to the axon growth mode and are scarcely sensitive to culture conditions, indicating that the neuritic pattern expressed in vitro is largely determined by intrinsic stage-specific neuronal properties.

With increasing neuron age, apoE4 induced a loss of mature spines compared to apoE2 and apoE3, primarily via the loss of AMPAR from spines.

To investigate whether this apoE4-induced decrease in spine density results from alterations in the formation or the loss of dendritic spines, the effects of neuron age and apoE isoform on the total number and subclasses of spines were examined in long-term wild-type neurons co-cultured with glia from APOE2-, APOE3- and APOE4-TR mice.

In the current study, the effects of apoE isoform and neuron age on the density and composition of NMDAR and AMPAR on dendritic spines were examined in long-term wild-type (wt) neurons co-cultured with glia from APOE-TR mice.

Reduced lifespan in mutant LRRK2 (G2019S or R1441C)   [128] N2; baIn20 [P dat-1 ::LRRK2 (G2019S) + P dat-1 ::GFP] UA118 Dopaminergic neuron Age-dependent degeneration of DAergic neurons, behavioural deficit, locomotor dysfunction and depletion of dopamine(~72 % loss).

Our data suggest that aging neurons themselves, by developing a DDR-driven senescence-like phenotype, might become an important source of low-level, chronic pro-inflammatory and pro-oxidant signalling and thus a potential causal factor in brain and peripheral neuron aging.

The input layer consisted of seven neurons (age, gender and concentrations of aluminium, copper, iron, manganese and zinc).

As neurons age, they show signs of increased oxidative stress, disturbances in mitochondrial function, and accumulation of misfolded proteins, which are exacerbated in PD.

As neurons age, they show signs of diminished lysosomal and mitochondrial function, including increased oxidative stress and accumulation of misfolded proteins, and these changes become exacerbated PD.

This could well explain the progressive loss of regenerative potential as neurons age as well as the limited ability of CNS neurons to regenerate as compared to PNS neurons.

Interestingly, it has been reported that Top2b level decreases as neurons age (Bhanu et al., 2010) and Top2b deficiency can lead to dopaminergic neuron degeneration (Heng et al., 2012), further implicating a plausible role of Top2b in CNS degenerative diseases.