The study highlights the spatial strategies employed by staff to mitigate socio-spatial deficiencies in the healthcare environment.
Thus, it is not surprising that both entities, schizophrenia and MAM-exposed animals, present neuropathological anomalies in the entorhinal cortex (Table 2) as well as visuo-spatial deficiencies [115] [117].
Thus, an interesting question concerns how altered lamin A proteins cause disruption of the normal organization of the nuclear genome and how such spatial disruptions cause deficiencies in DNA repair processes even though DNA repair or metabolism genes are not defective.
A recent animal study reported that while the effects of chronic ethanol exposure (including working memory and episodic memory impairment) can recover with prolonged abstinence, the deficits of thiamine deficiency (spatial memory impairment and increased perseverative behavior) are more persistent [ 28].
Tet1 deficiency is associated with defects in neural development, altered expression of neuronal transcripts, and deficiencies in spatial learning and memory.
The spatial distribution of cholinergic deficiencies also appears to be different from AD, where deficits are most prominent in the temporal lobes while the thalamus is relatively spared [ 23].
At the same time, sub-lethal Zn deficiency induces spatial heterogeneous or interveinal chlorosis, development of reddish-brown or bronze tints and a range of auxin deficiency-like responses such as internode shortening, epinasty, inward curling of leaf lamina and reduction of leaf size [ 4- 9].
Furthermore, vitamin A deficiency impairs spatial memory [18], [19].
Transient MCAO induce a progressive deficiency in spatial performance related to impaired hippocampal function [ 22].
Mice with bilateral striatal 6-OHDA lesions displayed deficiency in spatial recognition with short, but not long, delay (De Leonibus et al., 2007).
