Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 53, Num. 1, 2005, pp. 59-59

Neurology India, Vol. 53, No. 1, January-March, 2005, pp. 59

Invited Comments

Invited Comments

Nagga Katarina

Department of Geriatric Medicine, University Hospital, SE-581 85 Linkoping
Correspondence Address:Department of Geriatric Medicine, University Hospital, SE-581 85 Linkoping
Email: katarina.nagga@lio.se

Related article: Clinical and laboratory features and response to treatment in patients presenting with vitamin B₁₂ deficiency-related neurological syndromes

Code Number: ni05015

It is today well known that vitamin B₁₂ deficiency can be associated with neuropsychiatric symptoms. Several studies have previously demonstrated that vitamin B₁₂ deficiency is more common in patients with dementia symptoms than in the cognitively non-impaired. This topic is touched upon in the article "Clinical and laboratory features and response to treatment in patients presenting with vitamin B₁₂ deficiency-related neurological syndromes" in the current issue of Neurology India. Vitamin B₁₂ deficiency increases with age and is present in 5-40% of the elderly population. However, the mechanism of neurological damage induced by a quantitative or functional vitamin B₁₂ deficiency is still unclear.

Vitamin B₁₂ exerts its physiological effect on two major enzymatic pathways: the conversion of homocysteine to methionine and the conversion of methylmalonyl coenzyme A to succinyl coenzyme A. Disruption of either of these pathways due to vitamin B₁₂ deficiency results in an elevation of both serum homocysteine and methylmalonic acid. Homocysteine levels are also elevated in the case of folate deficiency. Serum homocysteine is proposed to be more sensitive for functional intracellular vitamin B₁₂ deficiency than analysis of vitamin B₁₂ in serum.[1] Hence, homocysteine, vitamin B₁₂, and folate are closely linked together in the so-called one-carbon cycle. The proposed mechanism relates to the methylation reactions involving homocysteine metabolism in the nervous system.[2] Smith[3] has suggested that the brain suffers from a double whammy from hyperhomocysteinaemia: cerebrovascular damage that triggers or potentiates the effect of Alzheimer pathology combined with a direct neurotoxic effect of homocysteine.

There is an ongoing debate about the contribution of vitamin B₁₂ deficiency to the dementia syndrome. The current article adds to those finding an effect on cognitive function as a result of vitamin B₁₂ treatment in patients with cognitive impairment and co-occurring vitamin B₁₂ deficiency. One of the most intriguing findings in the study is the low mean age of the investigated subjects. It must be considered unexpected to find such a high percentage of cases with cognitive symptoms in ages below 65 years. It would be very interesting to see added neuropsychological data on the dementia cases, to elucidate exactly in what cognitive domains there was an improvement. It is possible that such a study might contribute to a better understanding of role of vitamin B₁₂ deficiency in dementia evolution.

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