Females have greater incidence rates in non-familial, sporadic late-onset Alzheimer disease (LOAD), when neuroprotective effects of oestrogen begin to diminish. This sex difference is well established in genetic epidemiology. In case it is not a familial and more strictly genomic based dementia subtype, or vascular dementia, often combined with LOAD, in the literature, there is no specific post-menopausal MCI or LOAD entity. Oestrogen level is simply one of the well-established LOAD risk factors, such as MetS components, sedentary life style, educational attainment, SES, nutritional factors, physical and mental activity and so forth. Re first question, usually there is a strong determinism of progression of MCI towards AD manifestation, but clinical literatures describe also forth-and-back switching until final loss of executive functions. Altogether, post-mortem studies find about 30-40% brains with strong senile amyloid placques, but who never showed AD signs during life time. According to current theorising, levels of oxidative stress, mitochondrial dysfunction, neuroinflammatory processes etc. are considered as decisive for MCI-LOAD manifestation, together with underlying genetic and epigenetic risks. These general neurodegenerative pathophysiological processes do not appear to be sex-specific.

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