Is there a neuropathology difference between mild cognitive impairment and dementia?
- PMID: 19585952
- PMCID: PMC3073531
- DOI: 10.31887/DCNS.2009.11.2/vharoutunian
Is there a neuropathology difference between mild cognitive impairment and dementia?
Abstract
The number of studies that have investigated the neuropathology of mild cognitive impairment (MCI) is small, but growing. In this paper we have restricted our focus to the consideration of the presence and extent of postmortem findings relevant to the neuropathology of Alzheimer's disease. We have drawn from studies that have investigated the postmortem neurobiology of the brains of persons with cognitive function at the interface between unimpaired normal function and mild but definite dementia. The data derived from these studies suggest that i) the brains of persons with MCI evidence significant neuropathological and neurobiological changes relative to those without cognitive impairment; ii) in general, the neuropathological and neurobiological changes are qualitatively similar to those observed in the brains of persons with frank AD-like dementia; and iii) the neuropathological and neurobiological brain changes associated with MCI are quantitatively less than those of persons who meet criteria for dementia. Thus, the available, albeit limited, data suggests that MCI is associated with the early stages of the neurobiological and neuropathological changes that culminate in the florid lesions of AD; including the accumulation of neuritic plaques, neurofibrillary tangles, synaptic and neurotransmitter associated deficits, and significant neuronal cell death.
El número de estudios que han investigado la neuropatología del deterioro cognitivo leve (DCL) es pequeño, pero creciente. En este artículo el foco de atención se ha centrado en la presencia y extensión de los hallazgos postmortem relevantes en la neuropaiología de la Enfermedad de Alzheimer (EA). Se ha recurrido a estudios que han investigado la neurobiología postmortem de cerebros de personas con función cognitiva en la interfaz entre la función normal sin deterioro y la demencia confirmada, pero leve. Los datos derivados de estos estudios sugieren que: 1) los cerebros de personas con DCL evidencian cambios neuropatológicos y neurobiológicos significativos en relación con los sujetos sin deterioro cognitivo, 2) en general, los cambios neuropatológicos y neurobiológicos son cualitativamente similares a los observados en los cerebros de personas con franca demencia tipo EA y 3) los cambios cerebrales neuropatológicos y neurobiológicos asociados con el DCL son cuantitativamente menores que los de personas que cumplen los criterios para demencia. Por lo tanto, la información disponible - aunque limitada- sugiere que el DCL está asociado con las etapas précoces de los cambios neurobiológicos y neuropatológicos que culminan en las lesiones floridas de la EA, incluyendo la acumulación de placas neuríticas, ovillos neurofibrilares, déficit sináptico y de neurotransmisores asociados, y signíficativa muerie celular neuronal.
Le nombre d'études ayant analysé la neuropathologie du déficit cognitif léger (DCL) est faible mais croissant. Cet article s'intéresse exclusivement à l'existence et à l'importance des observations postmortem applicables à la neuropathologie de la maladie d'Alzheimer (MA). Nos conclusions sont issues d'études ayant analysé la neurobiologie postmortem de cerveaux de personnes souffrant d'une fonction cognitive intermédiaire entre une fonction normale non altérée et une démence légère mais constituée. Les données issues de ces études montrent: 1) les cerveaux des personnes ayant un DCL manifestent des changements neuropathologiques et neurobiologiques significatifs en comparaison de ceux indemnes de déficit cognitif; 2) en général, les changements neuropathologiques et neurobiologiques sont qualitativement identiques à ceux observés dans les cerveaux de personnes ayant une démence franche semblable à la MA ; et 3) les modifications cérébrales neuropathologiques et neurobiologiques associées à la DCL sont quantitativement moins importantes que celles des personnes atteintes de démence. Ainsi, les données disponibles, bien que limitées, suggèrent que le DCL est associé aux stades précoces des changements neuropathologiques et neurobiologiques qui mènent aux lourdes lésions de la MA, comprenant une accumulation de plaques seniles, des dégénérescences neurofibrillaires, des déficits associés aux synapses et aux neuroiransmetteurs et une mort cellulaire neuronale significative.
Similar articles
-
The Contribution of Cerebral Vascular Neuropathology to Mild Stage of Alzheimer's Dementia Using the NACC Database.Curr Alzheimer Res. 2020;17(13):1167-1176. doi: 10.2174/1567205018666210212160902. Curr Alzheimer Res. 2020. PMID: 33583381 Free PMC article.
-
Neuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease.Neurobiol Aging. 2009 Jul;30(7):1026-36. doi: 10.1016/j.neurobiolaging.2009.04.002. Epub 2009 Apr 18. Neurobiol Aging. 2009. PMID: 19376612 Free PMC article.
-
Cortical neuritic plaques and hippocampal neurofibrillary tangles are related to dementia severity in elderly schizophrenia patients.Schizophr Res. 2010 Jan;116(1):90-6. doi: 10.1016/j.schres.2009.10.013. Schizophr Res. 2010. PMID: 19896333 Free PMC article.
-
Asymptomatic Alzheimer's disease: a prodrome or a state of resilience?Curr Alzheimer Res. 2011 Jun;8(4):330-5. doi: 10.2174/156720511795745348. Curr Alzheimer Res. 2011. PMID: 21222594 Free PMC article. Review.
-
Neuropathological diagnosis of Alzheimer's disease: a perspective from longitudinal clinicopathological studies.Neurobiol Aging. 1997 Jul-Aug;18(4 Suppl):S21-6. doi: 10.1016/s0197-4580(97)00065-1. Neurobiol Aging. 1997. PMID: 9330981 Review.
Cited by
-
Atrophy of amygdala and abnormal memory-related alpha oscillations over posterior cingulate predict conversion to Alzheimer's disease.Sci Rep. 2016 Aug 22;6:31859. doi: 10.1038/srep31859. Sci Rep. 2016. PMID: 27546195 Free PMC article.
-
Aging the brain: multi-region methylation principal component based clock in the context of Alzheimer's disease.Aging (Albany NY). 2022 Jul 30;14(14):5641-5668. doi: 10.18632/aging.204196. Epub 2022 Jul 30. Aging (Albany NY). 2022. PMID: 35907208 Free PMC article.
-
Mild cognitive impairment in Parkinson disease: heterogenous mechanisms.J Neural Transm (Vienna). 2013 Jan;120(1):157-67. doi: 10.1007/s00702-012-0771-5. Epub 2012 Feb 18. J Neural Transm (Vienna). 2013. PMID: 22350538 Review.
-
The Framingham Brain Donation Program: neuropathology along the cognitive continuum.Curr Alzheimer Res. 2012 Jul;9(6):673-86. doi: 10.2174/156720512801322609. Curr Alzheimer Res. 2012. PMID: 22471865 Free PMC article.
-
Clinical features and multidisciplinary approaches to dementia care.J Multidiscip Healthc. 2011;4:125-47. doi: 10.2147/JMDH.S17773. Epub 2011 May 15. J Multidiscip Healthc. 2011. PMID: 21655340 Free PMC article.
References
-
- Graham JE., Rockwood K., Beattie BL., et al. Prevalence and severity of cognitive impairment with and without dementia in an elderly population. Lancet. 1997;349:1793–1796. - PubMed
-
- Fisk JD., Merry HR., Rockwood K. Variations in case definition affect prevalence but not outcomes of mild cognitive impairment. Neurology. 2003;61:1179–1184. - PubMed
-
- Reisberg B., Ferris SH., Deleon MJ., Crook T. The Global Deterioration Scale for Assessment of Primary Degenerative Dementia. Am J Psychiatry. 1982;139:1136–1139. - PubMed
-
- Flicker C., Ferris SH., Reisberg B. A 2-year longitudinal-study of cognitive function in normal aging and Alzheimers-disease. J Geriatr Psychiatry Neurol. 1993;6:84–96. - PubMed
-
- Kluger A., Ferris SH., Golomb J., Mittelman MS., Reisberg B. Neuropsychological prediction of decline to dementia in nondemented elderly. J Geriatr Psychiatry Neurol. 1999;12:168–179. - PubMed
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Medical