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Even in mild cognitive impairment there are already abnormalities in sleep architecture and electroencephalography measures. Sleep changes in patients with amnestic mild cognitive impairment may contribute to memory deficits by interfering with sleep-dependent memory consolidation.⁸⁸In a small study, Ju investigated sleep in 145 cognitively healthy probands older than 45 years. Amyloid deposition, as assessed by β-amyloid levels, was present in 32 participants. This group had worse sleep quality, as measured by sleep efficiency compared with those without amyloid deposition, after correction for age, sex, and ApoE4 allele carrier status, while the quantity of sleep did not differ between groups. Frequent napping, 3 or more days per week, was associated with amyloid deposition. The authors concluded that indices for amyloid deposition in the preclinical stage of AD appears to be associated with worse sleep quality.⁸⁹Taken together the brain activity patterns may directly modulate the molecular cascades that are relevant to diseases. In the case of AD, increased resting-state activity may accelerate the formation of amyloid pathology. This opens up perspectives for new interventions that may take the form of a therapy that attempts to modify glycolysis or other aspects of brain metabolism or to boost prophylaxis by the promotion of healthy sleep behavior or working behavior.For the clinician the easily applicable neuropsychological test batteries augmented by a test for olfactory recognition continue to be at the heart of the diagnostic process for dementias, although new methods like CSF analyses or MRI volumetry are increasingly available and validated for clinical use. The use of amyloid-tracer PET or fMRI to investigate, for example, the DMN are still more preclinical than clinical in character. Despite enormous progress in our knowledge of some pathophysiologic mechanisms in the last decade, we are still far from understanding AD and also probably from finding a cure. The available medications or medications may, however, help us to manage some symptoms for our patients, and gain some time for them. To date the recent scientific advancements primarily offer earlier diagnosis. With new diagnostic criteria properly applied, we will likely be able to diagnose Alzheimer's disease many years before any relevant impairment is experienced by the patient. In light of the fact that most of us would suffer from AD, were we only to get old enough, one question arises: when the gods put the diagnosis before the therapy, how much “before” did they actually mean? As a clinician, I would appreciate any measure of “momentum” that would help me to translate biomarker findings, eg, a positive amyloid scan in PET, to the patient.