Suboptimal Baseline Serum Vitamin B12 Is Associated With Cognitive Decline in People With Alzheimer’s Disease Undergoing Cholinesterase Inhibitor Treatment

Abstract

ObjectivesCholinesterase inhibitors (ChEIs) are the mainstream treatment for delaying cognitive decline in Alzheimer’s disease (AD). Low vitamin B12 is associated with cognitive dysfunction, and its supplementation has been applied as the treatment for certain types of reversible dementia. The present study hypothesized that baseline serum vitamin B12 is associated with the deterioration of cognitive function in people with AD undergoing ChEI treatment.Materials and methodsBetween 2009 and 2016, medical records from 165 Taiwanese with mild to moderate AD who underwent ChEI treatment for at least 2 years were reviewed. Their baseline serum vitamin B12 levels were measured before treatment initiation. Their cognitive function was assessed using the Mini–Mental State Examination (MMSE) and Cognitive Abilities Screening Instrument (CASI). Student’s t test and multivariable logistic regression were used to analyze the association between cognitive decline and vitamin B12 level. Statistical analyses were performed using SPSS 19.0.ResultsOverall, 122 participants were women. Their median age was 76 years (ranging from 54 to 91). For people with optimal baseline vitamin B12 (above the median level of 436 ng/L), the rates of MMSE and CASI decline were 0.78 ± 1.28 and 2.84 ± 4.21 per year, respectively, which were significantly slower than those with suboptimal vitamin B12 (1.42 ± 1.67 and 4.94 ± 5.88 per year; p = 0.007 and 0.009, respectively). After adjustment for age, sex, education level, hypertension, diabetes, history of stroke, and baseline cognitive function, the baseline serum vitamin B12 level was negatively associated with MMSE and CASI decline.ConclusionSuboptimal baseline serum vitamin B12 level is associated with cognitive decline in people with AD undergoing ChEI treatment.

Nutrition is a hard science

“…Physicians cannot serve their patients without preparing extensively to understand and deal with at least the most typical nutritional scenarios in practice. Will they know enough to understand that vitamin B 12 deficiency can accelerate the cognitive decline of their elderly patient in the early stages of Alzheimer’s disease, 5 and will they be ready to initiate the appropriate assessments and interventions? What about exposure to nitrous oxide during routine anaesthesia or for recreational purposes 6 ?…”

Neuroprotectors in the correction of cognitive impairment

“…Витамин В 12 участвует в строительстве белковых и жировых структур защитного миелинового слоя, производстве метионина [15]. Диметилглицин (витамин В 16 ) -один из доноров метильной группы. Перенос метильных групп используется организмом во многих биохимических реакциях, среди которых -детоксикация клеток, образование фосфолипидов, обезвреживание токсинов клетками и восстановление ДНК, синтез ацетилхолина, являющегося главным нейромедиатором памяти и интеллекта, а также важным нейротрансмиттером вегетативной нервной системы.…”

“…Значительное число исследований посвящено изучению эффективности применения витаминов группы В с целью предупреждения прогрессирования когнитивных нарушений. В одном из них [16] было высказано предположение, что когнитивные нарушения могут быть связаны с низким уровнем витамина B 12 в сыворотке крови (1,42±1,67 нмоль/л). Авторами была выдвинута гипотеза, согласно которой базовый уровень витамина В 12 в сыворотке крови связан с ухудшением когнитивной функции у пациентов с БА.…”

“…Одним из препаратов, включающим все витамины группы В: В 1 (тиамина гидрохлорид), В 2 (рибофлавин), В 6 (пиридоксина гидрохлорид), В 8 (инозитол), В 9 (фолиевая кислота), В 12 (цианокобаламин), В 16 (диметилглицин гидрохлорид), а также гинкго билоба и ФХ, является церебровин («Novator Pharma», Великобритания), зарегистрированный в России.…”

Epigenetic Factors in Late-Onset Alzheimer&rsquo;s Disease: <em>MTHFR</em> and<em> CTH </em>Gene Polymorphisms, Metabolic Trans-sulfuration and Methylation Pathways, and B Vitamins

“…Other causes of B12 deficiency include atrophic body gastritis, malabsorption of vitamin B12, gastrectomy, gastric bypass or other bariatric surgery, inflammatory bowel disease, tropical sprue, use of metformin, anticonvulsants, drugs to block stomach acid, and vegetarian diets low in meat and dairy products. Hemodialysis patients, nitrous oxide inhalation, and cholinesterase inhibitors in LOAD patients[87] also increase the risk of vitamin B12 deficiency. Epidemiological studies have shown that prevalence of vitamin B12 deficiency increases with age[88,89], due to decreased saliva (dry eyes-dry mouth) and gastric atrophy with deficits respectively of haptocorrin and intrinsic factor.…”