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• W1680312384 abstract "In 1982, Beck et al.1 warned us of the coming “silent epidemic” of Alzheimer's disease (AD) cases. As the baby boomers retire, the number of dementia cases will increase dramatically, but it is now less clear that they will suffer from AD. Instead, ischemic cerebral vasculopathy (ICVD) appears increasingly likely to play a major role in late-onset dementias “of the Alzheimer's type.” The comorbid association between clinically diagnosed AD and ICVD is well established; 60% of cases of senile dementia of the Alzheimer's type may have ICVD.2 Such lesions appear to reduce the burden of AD pathology associated with the diagnosis of dementia.3 AD pathology can be conveniently summarized in terms of six Braak stages.4 These range from no AD pathology (Braak Stage 0) to pan-cortical involvement (Braak Stage VI). The hippocampus is involved at about Stage III.4 It has been shown that clinicians generally fail to diagnose dementia until the disease reaches a few specific regions of interest (ROIs) that are affected between Stages IV and V.5 However, this is in the absence of ICVD. The Braak stage of demented cases is inversely related to the severity of comorbid ICVD.6 In our cases, only those with comorbid ICVD were diagnosed with dementia in advance of these critical ROIs.5 This is interesting because the critical ROIs were all related to the frontal cortical substrates of executive control function (ECF);5 the same ROIs have been implicated as the essential substrates of vascular dementia;7 lesions of the subcortical elements of certain frontostriatothalamic circuits (and their associated anterior white matter tracts), which vicariously affect the critical cortical ROI via diaschisis, can impair ECF;8, 9 and these subcortical frontal system elements are disproportionately vulnerable to ICVD. Notice that the word “stroke” has not been used in describing this situation. Stroke refers to a clinical syndrome that overlaps, but is not synonymous with, ICVD. In this issue of the Journal of the American Geriatrics Society, Schmidt et al.10 report that 12.7% of an elderly community sample present with objective evidence of ICVD (using magnetic resonance imaging (MRI)) but without a clinical history of stroke. Such “silent strokes” (an oxymoron) were associated with ICVD risks and objective impairments in cognition, procedural speed, and motor performance. It is interesting to note that 53.2% of these silent lesions were associated with elements of the frontal circuits, including the basal ganglia (36.2%), frontal lobe (8.5%), and thalamus (8.5%). Moreover, the true prevalence of silent ICVD-related cognitive impairment may be much higher than that reported by Schmidt et al.10 This is because the ischemic lesions most strongly associated with cognitive impairment are too small to be imaged using MRI. Another study, using data from the Honolulu Asian Aging Study, examined the association between four types of ICVD at autopsy and premorbid cognitive testing.11 Only microvascular changes (ICVD lesions visible only using light microscopy) contributed significantly to the variance in performance on the Cognitive Abilities Screening Instrument. No other ICVD lesion, including leukoariosis, large-volume (>1 mL) stroke or hemorrhage, or small-volume lacunas (≤1 mL), contributed to cognition independently of such microvascular lesions. Most importantly, it was again the subset of microvascular lesions in frontal circuits (frontal cortex, caudate, putamen, internal capsule, and thalamus) that accounted for most of the variance in cognitive function. Thus, the frontal system lesions detected by Schmidt et al. are best considered as proxies for more clinically relevant microvascular lesions that cannot be imaged. I leave the reader to ponder two interesting issues raised by these observations. First, why is it that clinicians do not clinically recognize frontal-circuit ICVD? I believe it is because we are most familiar with the motor and sensory effects of more posterior, generally embolic, central nervous system lesions. Clinicians are not currently being adequately trained to detect the cognitive and behavioral sequelae of executive impairment, nor do they routinely screen for such impairment with bedside measures. Second, if it is conceded that clinicians do not adequately recognize ECF impairments, how then do they categorize the dementias that develop from frontal system ICVD, especially if it is superimposed on preclinical Braak stages? I believe they diagnose many such cases as “AD.” There is good reason to suspect that the comorbid occurrence of frontal system ICVD and preclinical AD is particularly common after the age of 70. This may explain the persistent identification of stroke risks as predictors of incident “AD,”12 the high prevalence of ICVD in clinically diagnosed “AD” cases,13 the weakened association between apolipoprotein ɛ4 and dementia risk in octogenarians,14 the failure of many AD cases ever to reach the highest Reisberg stages,15 and the low specificity at autopsy of a clinical diagnosis of AD made after age 79.16 Because octogenarians are the most rapidly growing segment of the U.S. population17 and are disproportionately represented among incident AD cases,18 frontal system ICVD may ironically account for the majority of future AD cases. In fact, ICVD may be the most common mechanism by which persons aged 70 and older with mild cognitive impairment convert to AD. We are truly facing a new silent epidemic. Dr. Royall is supported by Eisai, Bristol-Meyers Squibb, Celgene Corporation, Forrest Laboratories, and Janssen." @default.
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• W1680312384 date "2004-06-15" @default.
• W1680312384 modified "2023-10-17" @default.
• W1680312384 title "The New “Silent” Epidemic" @default.
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• W1680312384 doi "https://doi.org/10.1111/j.1532-5415.2004.52325.x" @default.
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