Abstract

Alzheimer's disease (AD) is the main cause of dementia, affects 17-20% of people > 65 years and 50% > 85 years. AD only appears in late adulthood, and the risk to develop the disease doubles every 5 years after age 65. Heritability for AD is estimated to explain between half of total AD cases. Almost half of AD being attributable to non-genetic risk factors in which epigenetics mechanisms are supposedly involved. Expression with epigenetics has been ignored in clinical practice. Early detection and treatment may delay the full blown expression of the more grave disease of memory loss like AD. A consecutive cohort of 183 patients to present to neurology clinic was included; Set of blood test and Montreal Cognitive Assessment (MoCA) screening for the work of neurological complaint.ANA immunoassay and titer> 1:40 with positive and type, Vit B12 level < 300, folate <6. Vit D level <30, CRP>.05 Homocystine level >12 were positive. MoCA score of < 26 was MCI 25-20, 20–15 moderate & <15 sever memory loss. M:F, age 16 to 92 yrs. Vitamin B12 levels are significantly correlated with their homocysteine levels (t = −3.6375, df = 13, p-value = 0.003008). For every 1 umol/L increase in homocysteine, there is a 6.652 pg/mL decrease in Vitamin B12. In addition, Homocysteine levels are significantly linearly related with their MoCA scores (t = −3.9187, df = 141, p-value = 0.0001383). For every 1 umol/L increase in Homocysteine levels, there is a .25025 decrease in MoCA scores. In terms of Vitamin D, the data provides evidence that patients’ Vitamin D levels are significantly correlated with their MoCA scores (t = 2.6162, df = 44, p-value = 0.01214). For every 1 increase in Vitamin D, there is a 0.3455 increase in MoCA scores. Mean MoCA score for patients who are ANA positive is significantly less than 26 (t = −2.6437, df = 17, p-value = 0.008532). Active vigilance and early intervention with simple treatable cause of memory loss may delay the onset of dementia and AD.

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