Alzheimer's disease with and without cerebral infarcts

Ser, Teodoro del; Hachinski, Vladimir; Merskey, Harold; Muñoz, David G.

doi:10.1016/j.jns.2004.08.016

Cited by 47 publications

(26 citation statements)

References 63 publications

(104 reference statements)

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“…In our study, the only risk factors related to microinfarcts were history of TIA and to a lesser extent a history of stroke. Some studies[16, 26], but not all[30], have found hypertension to be a risk factor for microinfarcts. In the BLSA, severe hypertension (lasting 10 years, requiring two or more medications, and systolic blood pressure >160mm Hg) was related to the presence of microinfarcts[16].…”

Section: Discussionmentioning

confidence: 99%

Microinfarcts are common and strongly related to dementia in the oldest‐old: The 90+ study

Corrada

Sonnen

Kim

et al. 2016

Alzheimer's & Dementia

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INTRODUCTION We estimated the prevalence of microinfarcts and their association with dementia in a cohort of oldest-old participants. METHODS Participants were from The 90+ Study, a population-based study of people 90 and older. Dementia diagnoses were assigned post-mortem during a consensus conference. Microinfarcts were evaluated in six brain regions. RESULTS At death, the 213 participants were on average 97 years old, 69% were women, and 52% had dementia. 51% of participants had microinfarcts and 17% had 3+ microinfarcts. The odds ratio (OR) for dementia was similar for 3+ microinfarcts (OR=4.75, p<0.01) and tangle stage V-VI (OR=4.70, p<0.001). Only microinfarcts in cortical regions (other than occipital) were associated to dementia. DISCUSSION In this oldest-old cohort, microinfarcts are common and contribute independently and similarly in magnitude to dementia as tangles. As risk factors for microinfarcts and other dementing pathologies are likely to differ, identifying these factors is crucial to developing prevention strategies for dementia in the oldest-old.

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Section: Discussionmentioning

confidence: 99%

Microinfarcts are common and strongly related to dementia in the oldest‐old: The 90+ study

Corrada

Sonnen

Kim

et al. 2016

Alzheimer's & Dementia

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“…In that context, which seems quite representative of incident AD, one third of the patients (32.5%) qualified for the ADVC group. Autopsy-proven studies demonstrated a range of prevalence of cerebrovascular lesions in AD from 39 to 68% [1,2,3,4,7] and that variability mostly depended on differences in the kind of studied vascular lesions (macroscopic infarcts, microscopic infarcts, etc.). Our patients displayed an inferior prevalence of cerebrovascular disease possibly due to the low sensitivity of ADVC working definition or, in the autopsy-proven studies, due to accumulation of cerebrovascular pathology near death.…”

Section: Discussionmentioning

confidence: 99%

“…Evidence from clinicopathological studies demonstrated that multiple brain pathologies usually coexist in old people with dementia, and that was particularly the case for the combination of Alzheimer's disease (AD) and cerebrovascular lesions [1,2,3]. Persons with multiple pathologies were also more likely to exhibit dementia during life, compared with persons with a single diagnosis [4].…”

Section: Introductionmentioning

confidence: 99%

Alzheimer’s Disease with Vascular Component: A Distinct Clinical Entity

Olazarán

Navarro

Rojo

2012

Dement Geriatr Cogn Disord Extra

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Background: Longitudinal reports on the clinical features of patients with Alzheimer’s disease (AD) and concomitant cerebrovascular disease are scarce. Methods: We elaborated a working definition of AD with vascular component (ADVC), and this definition was retrospectively investigated in a cohort of patients with cognitive deterioration who were prescribed a cholinesterase inhibitor during usual practice. Results: A total of 137 patients with probable AD and 66 patients with ADVC were studied during a mean follow-up period of 2.8 years. Univariate analyses demonstrated worse functional evolution and anticipation of psychotic symptoms and agitation in the ADVC group. Conclusions: The present results are consistent with an additive model of predominantly frontal-subcortical vascular damage in AD.

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“…The severity of β amyloid load in the brain is not significantly influenced by CVD except for a shift from Aβ-40 to Aβ-42 in the thalamus of elderly subjects, the reason of which is unknown [110], while other authors found accumulation of brain Aβ increasing with age in VaD subjects more than in elderly without CVD [123]. In general, there are no major differences in neurodegenerative lesion load between AD and AD + CVLs, except when these are located in the temporal lobe and hippocampus, suggesting that this location may be important in the pathophysiology of both VaD and mixed AD + vascular dementia [124]. The pathology of mixed dementia has been reviewed recently [see 51,125], and the thresholds for vascular and degenerative lesions for distinguishing "pure" VaD or AD from mixed cases have been critically discussed [126].…”

Section: Cerebrovascular Lesions and Alzheimer Diseasementioning

confidence: 93%