Increasing incidence of dementia in the oldest old: evidence and implications
ABSTRACT The oldest old are the fastest growing segment of the US population but accurate estimates of the incidence of dementia in this age group have been elusive. Corrada and colleagues present data on the 5-year age-specific rates of dementia incidence in persons 90 years and older from The 90+ Study. Their findings show a continued exponential increase in dementia incidence after age 90 that mirrors the increase observed in persons aged 65 to 90, with a doubling every 5.5 years. This contrasts with previous smaller studies reporting a slowing of the increase in incidence after age 90. If confirmed, the continued increase, rather than a plateau, in the incidence of dementia in the oldest old has implications for proper healthcare planning. Strategies for prevention and treatment will require more information regarding risk factors and the etiopathogenesis of dementia in the oldest old.
Full-textDOI: · Available from: Julie A Schneider, Jun 16, 2015
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ABSTRACT: Vascular cognitive impairment (VCI) [vascular cognitive disorder (VCD), vascular dementia] describes a continuum of cognitive disorders ranging from mild cognitive impairment (MCI) to dementia, in which vascular brain injury involving regions important for memory, cognition and behavior plays an important role. Clinical diagnostic criteria show moderate sensitivity (ca 50%) and variable specificity (range 64-98%). In Western clinical series, VaD is suggested in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series varies from 0.03 to 58%, with means of 8 to 15% (in Japan 22-35%). Major types of sporadic VaD are multi-infarct encephalopathy, small vessel and strategic infarct type dementias, subcortical arteriosclerotic leukoencephalopathy (SAE) (Binswanger), multilacunar state, mixed cortico-subcortical type, granular cortical atrophy (rare), postischemic encephalopathy, and a mixture of cerebrovascular lesions (CVLs). They result from systemic, cardiac and local large or small vessel disease (SVD); their pathogenesis is multifactorial. Hereditary forms of VaD caused by gene mutations are rare. Cognitive decline is commonly associated with widespread small ischemic vascular lesions involving subcortical brain areas (basal ganglia and hemispheral white matter). The lesions affect neuronal networks involved in cognition, memory, and behavior (thalamo-cortical, striato-subfrontal, cortico-subcortical, limbic systems). CVLs often coexist with Alzheimer-type lesions and other pathologies; 25-80% of elderly demented show mixed pathologies. The lesion pattern of "pure" VaD differs from that in mixed dementia (AD + CVLs) suggesting different pathogenesis of both phenotypes. Minor CVLs, except for severe amyloid angiopathy, appear not essential for cognitive impairment in full-blown AD, while both mild AD-type pathology and SVD may interact synergistically in promoting dementia. However, in a large percentage of non-demented elderly individuals, both AD-related and vascular brain pathologies have been reported. Despite recent suggestions for staging and grading CVLs in specific brain areas, due to the high variability of CVLs associated with cognitive impairment, no validated neuropathological criteria are currently available for VaD and mixed dementia. Further clinico-pathological studies and harmonization of neuropathological procedures are needed to validate the diagnostic criteria for VaD and mixed dementia in order to clarify the impact of CVLs and other coexistent pathologies on cognitive impairment as a basis for further successful therapeutic options.Frontiers in Aging Neuroscience 04/2013; 5:17. DOI:10.3389/fnagi.2013.00017 · 2.84 Impact Factor
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ABSTRACT: The prevalence of both Alzheimer's disease (AD) and vascular dementia (VaD) increase with advancing age, but epidemiologic data above age 85 are imprecise and inconsistent. A retrospective hospital-based study of the prevalence and pathology of VaD was performed in 1700 consecutive autopsy cases of demented elderly in Vienna, Austria (mean age 84.3 ± 5.4 SD; 90% over age 70). It assessed clinical and general autopsy data and neuropathology including immunohistochemistry. Neuropathologic diagnosis followed current consensus criteria. Four age groups (7th to 10th decade) were evaluated. "Pure" VaD (due to cerebrovascular disease without other pathologies; neuritic Braak stages 1.2-1.6) was observed in 12.3% of the total cohort, decreasing between age 60 and 90+ from 15.0 to 8.7%. Morphologic subtypes (subcortical arteriosclerotic encephalopathy, multi-infarct encephalopathy, and strategic infarct dementia) showed no age-related differences. By contrast, AD (without concomitant pathologies; 45.6% of total), mixed dementia (AD + cerebrovascular encephalopathy; 5.5%), and AD with minor cerebrovascular lesions (22.3%) increased with age. The relative prevalence of AD + Lewy pathology (9.3%) remained fairly stable, whereas other dementias (5.0%) decreased significantly over age 90. 85% of the patients with "pure" VaD had histories of diabetes, 75% of stroke(s), 95% morphologic signs of hypertension, 65% myocardial infarction (recent and old ones), 97% cerebral hypertonic-arteriosclerotic microangiopathy (associated with cerebral amyloid angiopathy in 23%) and 90% severe atherosclerosis of large cerebral arteries. Similar autopsy findings were seen in mixed dementia (MIX) and in AD + minor cerebrovascular lesions. Major vascular lesions differed between VaD and MIX, VaD showing more than 60% subcortical infarcts, MIX only 43% such lesions. This retrograde hospital-based study using strict morphologic diagnostic criteria confirmed the existence of "pure" VaD in old age, with a tendency to decline after age 90, while AD and AD + cerebrovascular pathologies showed considerable age-related increase, and "pure" AD slightly decreasing after age 90.Journal of Alzheimer's disease: JAD 01/2010; 21(4):1283-93. DOI:10.3233/JAD-2010-100603 · 3.61 Impact Factor
- Journal of Cellular and Molecular Medicine 10/2010; 14(10):2415-6. DOI:10.1111/j.1582-4934.2010.01159.x · 3.70 Impact Factor