Abstract
Chronic kidney disease and Alzheimer’s disease are chronic conditions highly prevalent in elderly communities and societies, and a diagnosis of them is devastating and life changing. Demanding therapies and changes, such as non-compliance, cognitive impairment, and non-cognitive anomalies, may lead to supplementary symptoms and subsequent worsening of well-being and quality of life, impacting the socio-economic status of both patient and family. In recent decades, additional hypotheses have attempted to clarify the connection between these two diseases, multifactorial in their nature, but even so, the mechanisms behind this link are still elusive. In this paper, we sought to highlight the current understanding of the mechanisms for cognitive decline in patients with these concurrent pathologies and provide insight into the relationship between markers related to these disease entities and whether the potential biomarkers for renal function may be used for the diagnosis of Alzheimer’s disease. Exploring detailed knowledge of etiologies, heterogeneity of risk factors, and neuropathological processes associated with these conditions opens opportunities for the development of new therapies and biomarkers to delay or slow their progression and validation of whether the setting of chronic kidney disease could be a potential determinant for cognitive damage in Alzheimer’s disease.
Highlights
Recent studies have highlighted that cystatin C shows a controversial influence in the pathology of Alzheimer’s disease (AD); on the one hand, it appears to control the levels of Aβ that bind directly to Aβ and inhibit its aggregation, but on the other hand, as a substrate for cathepsin B protease, it appears to be competitive for Aβ degradation [142,143,144]
In most patients without broad cerebral white matter modifications, Mini Mental State Examination scores elevated or were maintained at 18 months follow-up. These findings suggest that cognitive decline as a consequence of cerebrovascular disease has not been improved by hemodialysis [156]
Prompt recognition and management of these mechanisms in first Chronic kidney disease (CKD) stages may signify a window of opportunity to diminish their influence at advanced stages
Summary
From a pathophysiological point of view, it is known that AD may have a vascular constituent, and the cause of cognitive decline is multifaceted. The degree of microvascular damage and the occurrence of microalbuminuria secondary to kidney injury may reveal comparable cerebral microvascular damage by disturbing the blood–brain barrier, the impairment of which causes protein leakage with cerebral white matter disease This has been supported by brain imaging studies, which showed that progression of AD is enhanced in individuals with increased cerebro-spinal fluid/plasma albumin ratio [62,63]. (sICAM-1), and sE-selectin were associated with reduced executive functioning and information processing speed in older subjects without [70] or with late-onset AD or vascular dementia [71] The results of these studies, in addition to the vascular hypothesis, support the idea that elevated levels of EA markers are primarily implicated in the pathogenesis leading to cognitive decline [72]
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