Decoding the complex nexus: the mechanistic interplay of hyperhomocysteinemia in brain aging and neurological disorders.

As ageing populations worldwide confront an increasing prevalence of neurological deficits, elucidating the underlying causes and associated factors has become paramount. The decline in age-related cellular processes precipitates neurodegeneration and cognitive decline, significantly impairing quality of life. Homocysteine (Hcy), a physiological amino acid resulting from protein catabolism, can lead to hyperhomocysteinemia (HHcy) when present at elevated levels. While the deleterious effects of high Hcy levels on arterial health and cardiovascular disease are well-documented, the connection between Hcy and brain diseases remains largely underexplored. Recent findings reveal that disruptions in Hcy metabolism, coupled with deficiencies in vitamin B12 along with folate can alter methylation as well as redox states, ultimately impacting calcium influx and contributing to the accumulation of amyloid and tau proteins. Severe undesired conditions like neuronal necrosis, and apoptosis may happen due to these biochemical signaling cascades. This paper aims to synthesize current knowledge regarding the potential role of HHcy in neurodegenerative diseases, drawing compelling connections among dietary methionine daily consumption, HHcy, oxidative stress, mitochondrial functioning, and accelerated epigenetic aging. By offering a comprehensive exploration of these interrelationships, we aspire to illuminate the critical need for further research in this domain, ultimately fostering innovative therapeutic strategies for eliminating the effect of HHcy upon neurological health.