Sentence examples for human dementia from inspiring English sources

This is shown in animal studies (Honarmand et al. 2014), human dementia studies (Leyhe et al. 2009), as well as in epilepsy samples.

All animal models used to study human neurodegenerative diseases consist of transgenic mice carrying mutant forms of genes shown to be involved in human dementia [24], [25], [26].

A serious limitation of these models is that their design is predicated on the assumption that development of amyloid plaques and neurofibrillary tangles is directly related to the cognitive and behavioral changes associated with human dementia.

Equally, in the animal models discussed above there has been no demonstration that the animals suffer from a condition that strictly reproduces human dementia.

To avoid many potential artefacts of the over expression models, we have produced a mouse model of human dementia genetically congruous to the human case.

Thus we favor this model for studies exploring the progression and treatment of WT tau driven tauopathies, which represent the majority of human dementia cases.

But some experts caution that the lack of tangles might mean that flies aren't a good model of human dementias.

Traditionally, mouse models for human dementias are based on a transgenic approach in which human mutant proteins that cause familial forms of dementia are over-expressed under the control of brain-specific promoters [25], [26], [27].

Age-related changes in circadian rhythmicity have become an important area of research, especially since cognitive dysfunctions in human dementias are often associated with circadian rhythm and sleep disorders.

These results suggest that sAPPβ and/or β-CTF, rather than Aβ, are the toxic species causing dementia, and indicate that reducing β-cleavage of APP is an appropriate therapeutic approach to treating human dementias.

Because fundamentally, ego is what makes us human, and dementia takes that very human self-interest away, drip by drip.