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EDITORIAL
Year : 2015  |  Volume : 63  |  Issue : 4  |  Page : 493--494

Metabolic syndrome: A smoldering risk to the cognition of the ageing Indian?

Anoop Varma 
 Department of Neurology, The Santokba Durlabhji Institute of Neurosciences, Santokba Durlabhji Memorial Hospital and Research Centre, Jaipur, Rajasthan, India

Correspondence Address:
Anoop Varma
Department of Neurology, The Santokba Durlabhji Institute of Neurosciences, Santokba Durlabhji Memorial Hospital and Research Centre, Jaipur, Rajasthan
India




How to cite this article:
Varma A. Metabolic syndrome: A smoldering risk to the cognition of the ageing Indian?.Neurol India 2015;63:493-494


How to cite this URL:
Varma A. Metabolic syndrome: A smoldering risk to the cognition of the ageing Indian?. Neurol India [serial online] 2015 [cited 2019 Nov 14 ];63:493-494
Available from: http://www.neurologyindia.com/text.asp?2015/63/4/493/161988


Full Text

Dementia is a major challenge. In 2010, there were 3.7 million Indians with dementia and estimates suggest a 150-200% increase in numbers over the next 15 years.[1] In addition to individual suffering, the implications of dementia for the family and society are incalculable and profound. With scanty social care or support systems, families remain the main carers. There is urgent need to combat this rising menace in every possible way. Most drug therapies for primary dementias are modest with little, if any, curative effect. It is thus incumbent on the health profession to lay greater emphasis on all possible preventative approaches. Over the last decade-and-a-half, the role of vascular risk in the etiopathogenesis of all forms of major dementias (including neurodegenerative e.g. Alzheimer's disease [AD]) has been recognized. [2] Ghosh et al. [3] examine an aspect of this link in the Indian population in this issue.

The study affirms greater cognitive dysfunction (based on 3MS scores) in patients over 60 with metabolic syndrome (metS). This work is cross-sectional and the authors themselves suggest longitudinal follow-up to evaluate progressive cognitive changes in metS groups. The second component of the study suggests a more severe cognitive dysfunction in patients with higher high-sensitivity C-reactive protein (hs-CRP) levels. The numbers are small (metS with high hs-CRP n = 20) for the study to be conclusive from these statistical observations.

It has been previously proposed that metS is associated with a low-grade inflammatory response. [4] In parallel, there is evidence to suggest that neuroinflammatory and neurodegenerative conditions may share common biological mechanisms. [5],[6] Focusing on metS causing cognitive dysfunction increases the possibility of identifying the risks that may lead to the development of frank dementias in subsequent years. If established, this would call for enhancing interventions that may prevent metS in the first place. Early and efficient strategies to reduce risk factors could only succeed on hard evidence. Effective policies and convincing educational endeavors may then do well against the currently metS-friendly social structures that are driven by a culture of immediate gratification and utilitarianism. This paper may be the much-needed stimulus for larger scale multicenter epidemiological studies in the Indian population to closely examine the link between metS, cognitive performance, mild cognitive impairment (MCI) and the major forms of primary dementias (AD, vascular dementia, dementia with Lewy bodies and frontotemporal lobar degeneration). It would be interesting to examine the socioeconomic backgrounds of these subjects. This may translate into policies that are global across all strata of healthcare, and not merely restricted to tertiary centers.

If low-grade inflammation is confirmed as an effect of metS that influences the development of cognitive impairment and/or dementia, it would argue for methods of interventions to prevent progression of a biological cascade that may otherwise lead to irreversible dementia. It is tantalizing to consider hs-CRP levels as a marker of cognitive impairment in metS subjects; unfortunately, this study at best is only indicative of such a possibility. A more detailed investigation with statistically sound numbers, using a wider plethora of markers of inflammation, may provide greater insights.

In contrast to a cross-sectional design, of greater significance would be documentation of serial observations of cognitive symptoms (if any) with robust longitudinal neuropsychological assessments in subjects with metS. Test scores are of value in documenting cognitive dysfunction. However, it is simplistic to translate statistical differences in test battery scores to denote "cognitive decline." Decline (vide "cognitive decline," Ghosh et al., [3] this issue) suggests deterioration over a period of time (the design au contraire is cross-sectional). The detection of statistical cognitive dysfunction in groups with metS, especially those with higher hs-CRP may not necessarily translate into a link with defined cognitive syndromes (e.g. MCI or dementias). Equally so, it must be acknowledged that interventions necessarily are best introduced prior to the development of these very clinical syndromes since pathogenesis and pathologies initiate years before the development of clinical manifestations. It is this reason that emphasizes the value of this attempt, despite pitfalls not uncommon in a pilot project. That metS may cause cognitive dysfunction is suggestive of a negative influence from components of metS on the normal mental faculty. Consequently growing evidence, including this study (relevant to the Indian population), of the role of metS in cognitive impairment argues for an immediate attention to these factors. The management of these very risks should prove most rewarding in the preclinical phases of cognitive disorders. For reasons cited above, longitudinal observations will clarify further the issues raised. It is tempting to imagine the development of scientifically robust interventions against these relentlessly cruel and progressive processes that eventually devour the very faculty that makes us human.

References

1ARDSI. The Dementia India Report 2010 Prevalence, Impact, Costs and Services for Dementia. New Delhi: Executive Summary Published by Alzheimer′s and Related Disorders Society of India; 2010.
2Stewart R. Vascular factors and Alzheimer′s disease. In: Ames D, Burns A, O′Brien J, editors. Dementia. 4 th ed. London: Hodder Arnold; 2010. p. 529-37.
3Ghosh A, Biswas AK, Banerjee A. A study on cognitive decline with respect to metabolic syndrome and inflammation in elderly Indians. Neurol India 2015;63:538-42.
4Misiak B, Leszek J, Kiejna A. Metabolic syndrome, mild cognitive impairment and Alzheimer′s disease - The emerging role of systemic low-grade inflammation and adiposity. Brain Res Bull 2012;89:144-9.
5Borjabad A, Volsky DJ. Common transcriptional signatures in brain tissue from patients with HIV-associated neurocognitive disorders, Alzheimer′s disease, and Multiple Sclerosis. J Neuroimmune Pharmacol 2012;7:914-26.
6Amor S, Puentes F, Baker D, van der Valk P. Inflammation in neurodegenerative diseases. Immunology 2010;129:154-69.