Alzheimer’s disease (AD), the foremost variant of dementia, has been associated with a menagerie of risk factors, many of which are considered to be modifiable. Among these modifiable risk factors is circadian rhythm, the chronobiological system that regulates sleep‐wake cycles, food consumption timing, hydration timing, and immune responses amongst many other necessary physiological processes. Circadian rhythm at the level of the suprachiasmatic nucleus (SCN), is tightly regulated in the human body by a host of biomolecular substances, principally the hormones melatonin, cortisol, and serotonin. In addition, photic information projected along afferent pathways to the SCN and peripheral oscillators regulates the synthesis of these hormones and mediates the manner in which they act on the SCN and its substructures. Dysregulation of this cycle, whether induced by environmental changes involving irregular exposure to light, or through endogenous pathology, will have a negative impact on immune system optimization and will heighten the deposition of Aβ and the hyperphosphorylation of the tau protein. Given these correlations, it appears that there is a physiologic association between circadian rhythm dysregulation and AD. This review will explore the physiology of circadian dysregulation in the AD brain, and will propose a basic model for its role in AD‐typical pathology, derived from the literature compiled and referenced throughout.

There is no question as to whether or not the beta amyloid (Aβ) peptide plays a role in the exacerbation and onset of AD. There are very evident correlations between the volume of Aβ deposition in the AD brain and the severity of the symptoms of AD-typical neurodegeneration. There are certainly many factors involved in the progression of AD, of which the aggregation of Aβ peptides is only one. While many have ruminated on the mechanism by which Aβ serves to impair synaptic function and contribute to neurodegeneration, the role of this protein has yet to be fully uncovered, not just in the AD brain, but in the normally functioning brain as well. Recent research has shed light on the role of Aβ in the normal brain, offering evidence for the fact that beta amyloid functions as an antimicrobial protein, with its primary objective being to serve an immunoresponsive purpose. This text will highlight some of the critical studies on the topic, and illuminate the role that Aβ most likely plays in the functioning of the normal brain, and how this influences its pathological deposition in the AD brain.

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