Sentence examples for mouse forebrain neurons from inspiring English sources

LRP seems to participate in the uptake and clearance of Aβ, because these processes are decreased when LRP1 is eliminated in mouse forebrain neurons (reviewed by Bu, 2009).

4– 6 As for REST, LRP6-Wnt signaling is decreased in autopsy brain tissue from AD patients and deletion of the Lrp6 gene selectively in mouse forebrain neurons enhances AD-like pathology.

Mice with only 30% of the wild-type COX activity in the brain, due to a deletion of the Surf1 gene, are nevertheless viable (45), and postnatal deletion of the Tfam gene in mouse forebrain neurons produces only a late-onset neurodegeneration, which manifests pathologically a full month after profound neuronal COX deficiency is seen histochemically (46).

Interestingly, in both Rett syndrome and in MeCP2-deficient mice, forebrain neurons exhibit a reduction in spine density [28].

A similar calculation can be performed for mouse forebrain cholinergic neurons using published estimates of the number of cell bodies in the nucleus basalis of Meynert (6632 and 4500), the volume of the mouse cortex as determined by MRI (109 mm), and the total length of cholinergic axons in the mouse cortex (1300 m), giving individual axon arbor length estimates of 20 cm and 29 cm (Table 1).

The total length of the axons in a P30 mouse forebrain cholinergic neuron arbor up to 50 cm is roughly 25 times the linear dimension of the mouse brain.

To target transgene expression to the forebrain neurons, these mice were crossed with mice expressing tTA via the CaMKII promoter [22] (Fig. 1A, B).

By employing SPG11 patient-derived forebrain neurons and mouse cortical neurons, this study provides the first evidence that SPG11 is implicated in axonal maintenance and cargo trafficking.

Since those PScDKO mice lack PS1 only in forebrain neurons, the findings may relate to the loss of PS2 in other cell types.

To study Drp1 in a neuronal population affected by Alzheimer's disease (AD), stroke, and seizure disorders, we postnatally deleted Drp1 from CA1 and other forebrain neurons in mice (CamKII-Cre, Drp1lox/lox (Drp1lox/lox

For in vivo analysis, we injected either generic AAV-GFP or conditional AAV-Stop-GFP to the hippocampus of adult (>2 months) wild-type mice (C57BL/6N) and Cre driver mice expressing Cre specifically in glutamatergic forebrain neurons under the control of regulatory sequences of the NEX gene (NEX-cre).