On basis of some studies, the authors suggest to reconsider the links between the decision making, in particular the under ambiguity one and the cognitive functions, questioning how executive functions contribute to this decision modality. Furthermore, the cortical neurodegenerative diseases seem to demonstrate that the decision under ambiguity may be impacted by the cognitive functions, challenging the assumed independency between these two processes. In Parkinson's disease, controversies appear to know whether the primitive decision impairment concerns the modality under risk or the one under ambiguity, as well as the question of the frontal striatal loops primitively damaged in this pathology pending.

Only the decision making under ambiguity appears to be responsive to the effects of usual aging, suggesting there would be a premature aging of the limbic loops. Nevertheless, the comparison of these hypothesis with the clinical data raises a certain number of controversies. Its neural substrate would be the limbic frontal striatal loops. In the second case, the decision is exclusively based on preliminary reinforcements (decision under ambiguity) and would be partially independent of cognitive functions. This modality is linked to the executive functions and its neural substrate would be the cognitive frontal striatal loops. This is because patients with pathological aging still maintain the ability to benefit from contextual cues, even in advanced stages of the disease (Adam et. In the first case, the decision is taken based on success probabilities and also as a result of preliminary reinforcements (decision under risk). Two decision modalities have been isolated, depending on whether the decision making is performed under explicit knowledge of the risks taken or not. It therefore implies a large interconnection of cortical and subcortical structures that are directly impacted by the neuroanatomical and neurochemical modifications that occur during the usual or the pathologic aging. Therefore, reduced SIRT6 activity may drive pathological age-related gene expression signatures in the brain.Decision making is a complex ability that is likely to be damaged in numerous psychiatric and neurologic disorders and also during the aging process. We thus argue that SIRT6 has a pivotal role in preventing age-related transcriptional changes in brains. It therefore implies a large interconnection of cortical and subcortical structures that are directly impacted by the neuroanatomical and neurochemical modifications that occur during the usual or the pathologic aging. One of these candidates is YY1, which we found to act together with SIRT6 regulating specific processes. We found that each of these gene expression categories is associated with specific transcription factors, thus serving as potential candidates for their category-specific regulation. Osteoporosis (OA) and Alzheimer's disease (AD) are two forms of pathological aging, sometimes entangled, including an over-risk of OP in AD and degradation of cognitive functions after OP fracture, but the link between These two pathologies remain poorly understood.

Our results define four gene expression categories that change with age in a pathological or non-pathological manner, which are either reversed or not by CR. It is recognized as a central mechanism for the regulation of aging. In addition, we traced these differences in human and mouse samples of Alzheimer’s and Parkinson’s diseases, healthy aging and calorie restriction (CR).

Here, we investigated the effect of aging in the recognition of social cues. In surveys, elderly people often report substantial declines in navigational abilities. Journal of Neuropathological Experimental Neurology, 1977, 36, 474487. How aging and preclinical dementia affect our sense of direction. To understand SIRT6 roles in transcript pattern changes, we analyzed transcriptomes of young WT, old WT and young SIRT6-KO mice brains, and found changes in gene expression related to healthy and pathological aging. Normal aging and many age-related disorders such as Alzheimer’ ss disease cause deficits in olfaction, however it is currently unknown how natural and pathological aging impact the detection of social odors which might contribute to the impoverishment of social behavior at old age further worsening overall health. Granulovascular degeneration in the aging brain and in dementia.

In the aging brain, SIRT6 levels/activity decline, which is accentuated in Alzheimer’s patients. Brain-specific SIRT6-KO mice present increased DNA damage, learning impairments, and neurodegenerative phenotypes, placing SIRT6 as a key protein in preventing neurodegeneration.

Pathological aging