The nectar produced by bees in nature is known as honey and has been consumed for its nutritional and medicinal properties. There is growing evidence that honey and its compounds have anti-inflammatory, antioxidant and anti-microbial properties that are relevant to the maintenance of health and the prevention of illnesses, including cardiocerebrovascular disease. Cerebral small vessel disease (CSVD) is one of the major risk factors for diseases such as stroke, dementia, Alzheimer’s disease, and Parkinson’s disease. CSVD is prevalent with aging and the presence of vascular risk factors. Its most common deleterious effect on the brain parenchyma is a neurological problem, causing a spectrum of subtle clinical manifestations such as neurocognitive dysfunction, emotional or behavioral disturbances, and gait dysfunction. Moreover, the pathological mechanisms and preventive strategies for CSVD remain elusive, which is reflected in the continued lack of effective therapeutic and preventive therapies. Given the growing literature on honey and its compounds as a superfood-based preventive measure, this narrative review highlights the neuroprotective potentials of honey and its compounds in relation to the current understanding of CSVD pathomechanism.
In this narrative review, we present the evidence on nucleotide-binding and oligomerization (NOD) domain-like receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome activation for its putative roles in the elusive pathomechanism of aging-related cerebral small vessel disease (CSVD). Although NLRP3 inflammasome-interleukin (IL)-1β has been implicated in the pathophysiology of coronary artery disease, its roles in cerebral arteriothrombotic micro-circulation disease such as CSVD remains unexplored. Here, we elaborate on the current manifestations of CSVD and its’ complex pathogenesis and relate the array of activators and aberrant activation involving NLRP3 inflammasome with this condition. These neuroinflammatory insights would expand on our current understanding of CSVD clinical (and subclinical) heterogenous manifestations whilst highlighting plausible NLRP3-linked therapeutic targets.
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