Coexisting Cerebral Infarction in Alzheimer's Disease Is Associated with Fast Dementia Progression: Applying the National Institute for Neurological Disorders and Stroke/Association Internationale pour la Recherche et l'Enseignement en Neurosciences Neuroimaging Criteria in Alzheimer's Disease with Concomitant Cerebral Infarction

Sheng, Bun; Cheng, Lik Fai; Law, Chun Bon; Li, Ho Lun; Yeung, Kwan Mo; Lau, Kwok Kwong

doi:10.1111/j.1532-5415.2007.01171.x

Cited by 28 publications

(20 citation statements)

References 21 publications

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“…1 Although some studies suggested that in patients with clinical Alzheimer's disease (AD), comorbid cerebrovascular disease was associated with a more rapid cognitive decline, 2,3 it is still unknown whether concurrent presence of Alzheimer's pathology is associated with a faster cognitive deterioration in patients with poststroke/TIA cognitive impairment.…”

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“…Our recent in vivo study using carbon-11-labeled Pittsburgh compound B ( 11 C-PiB) positron emission tomography (PET) found that ≈30% of subjects with poststroke/TIA cognitive impairment harbored Alzheimer's pathology.1 Although some studies suggested that in patients with clinical Alzheimer's disease (AD), comorbid cerebrovascular disease was associated with a more rapid cognitive decline, 2,3 it is still unknown whether concurrent presence of Alzheimer's pathology is associated with a faster cognitive deterioration in patients with poststroke/TIA cognitive impairment.In this study, we compared the longitudinal cognitive changes between VCI patients with and without AD-like amyloid-beta (Aβ) deposition measured using 11 C-PiB PET. We hypothesized that over 3 years, PiB-positive VCI (mixed VCI [mVCI]) subjects would experience a more rapid and continuous course of cognitive deterioration, resulting in more severe cognitive impairment than those who were PiB-negative (pure VCI [pVCI]).…”

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Influence of Amyloid-β on Cognitive Decline After Stroke/Transient Ischemic Attack

Liu

Wong

et al. 2015

Stroke

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C ognitive impairment in the context of stroke or transient ischemic attack (TIA) is a prototype of vascular cognitive impairment (VCI). Our recent in vivo study using carbon-11-labeled Pittsburgh compound B ( 11 C-PiB) positron emission tomography (PET) found that ≈30% of subjects with poststroke/TIA cognitive impairment harbored Alzheimer's pathology.1 Although some studies suggested that in patients with clinical Alzheimer's disease (AD), comorbid cerebrovascular disease was associated with a more rapid cognitive decline, 2,3 it is still unknown whether concurrent presence of Alzheimer's pathology is associated with a faster cognitive deterioration in patients with poststroke/TIA cognitive impairment.In this study, we compared the longitudinal cognitive changes between VCI patients with and without AD-like amyloid-beta (Aβ) deposition measured using 11 C-PiB PET. We hypothesized that over 3 years, PiB-positive VCI (mixed VCI [mVCI]) subjects would experience a more rapid and continuous course of cognitive deterioration, resulting in more severe cognitive impairment than those who were PiB-negative (pure VCI [pVCI]). Methods SubjectsSubjects of this study were participants of the ongoing Stroke Registry Investigating cognitive Decline (STRIDE) study. 1 In the Background and Purpose-We hypothesized that comorbid amyloid-beta (Aβ) deposition played a key role in long-term cognitive decline in subjects with stroke/transient ischemic attack. Methods-We recruited 72 subjects with cognitive impairment after stroke/transient ischemic attack to receive Carbon-11-labeled Pittsburgh compound B positron emission tomography. We excluded subjects with known clinical Alzheimer's disease. Those with and without Alzheimer's disease-like Aβ deposition were classified as mixed vascular cognitive impairment (mVCI, n=14) and pure VCI (pVCI, n=58), respectively. We performed Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment to evaluate global cognition and cognitive domains (memory, visuospatial function, language, attention, and executive function) at 3 to 6 months (baseline) and annually for 3 years after the index event. We compared cognitive changes between mVCI and pVCI using linear mixed models and analysis of covariance adjusted for age and education. Results-Over 3 years, there were significant differences between mVCI and pVCI on change of MMSE score over time (group×time interaction, P=0.007). We observed a significant decline on MMSE score (P=0.020) in the mVCI group but not in the pVCI group (P=0.208 6 were performed on subjects at 3 to 6 months (baseline) after the index event to index general cognition. Then subjects were further invited to return for annual follow-up. This study analyzed the data collected ≤3 years.This substudy included a sample of 72 subjects with cognitive impairment (CDR grade ≥0.5) from the STRIDE study. Clinical diagnoses were made by 2 neurologists specialized in dementia (V.C.T.M. and L.A.). Thirty-six subjects had CDR grade of ≥1 and met the criteria for dementia acco...

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Influence of Amyloid-β on Cognitive Decline After Stroke/Transient Ischemic Attack

Liu

Wong

et al. 2015

Stroke

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“…Likewise, Song et al (44) observed that AD with silent cerebral infarction showed a more severe cognitive decline than AD without vascular disease, indicating that cerebrovascular disease contributes to the severity of cognitive decline. Also, Sheng et al (45) showed that AD with coexisting cerebral infarction (satisfying criteria for VaD) was associated with faster progression of dementia. These findings suggest that prevention of cerebrovascular disease may play an important role in preventing the rapid cognitive decline of AD.…”

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Plasma homocysteine, apolipoprotein E status and vascular disease in elderly patients with mental illness

Nilsson

Gustafson²,

Nornholm³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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Background: Total plasma homocysteine (tHcy) concentration is increased in elderly patients with mental illness. Also, patients with vascular disease have significantly higher plasma tHcy concentration compared with patients without vascular disease. Apolipoprotein E (apoE) status is associated with cardiovascular disease and a major genetic risk factor is inheritance of the e4 allele. In the present study, we investigated the association between plasma tHcy and apoE status. Methods: The relation between apoE status, plasma tHcy and vascular disease was investigated in a cohort of consecutively enrolled elderly patients with mental illness (ns328). Results: Plasma tHcy concentrations were increased

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“…Current investigations have demonstrated a close link between sporadic Alzheimer's disease and ischemic brain episodes [6,43,44,47,50,53,63]. Additionally, earlier epidemiological studies noted that brain is chemia increased the incidence of sporadic Alzheimer's disease [15] and neurovascular risk factors for brain is chemia also raised the risk of sporadic Alzheimer's disease [58].…”

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Ischemia signalling to Alzheimer-related genes

Pluta

Kocki²,

Maciejewski³

et al. 2012

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A b s t r a c t In this paper we review the hard-earned data, which present ischemic induction of amyloid precursor protein, preseni lins, apolipoproteins and secretases genes, playing key roles in β-amyloid peptide generation. Presented data are strongly supporting a hypothesis that brain ischemia may be involved in the aetiology of sporadic Alzheimer's disease. Potential contribution and impact of ischemically activated genes on the development of sporadic Alzheimer's disease remain to be established at both genetic and functional levels. The identification of the genes involved in sporadic Alzheimer

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Abstract: In AD, co-occurrence of CI with distribution and severity as defined in the NINDS-AIREN neuroimaging criteria for VaD is associated with faster dementia progression.

Cited by 28 publications

References 21 publications

Influence of Amyloid-β on Cognitive Decline After Stroke/Transient Ischemic Attack

Influence of Amyloid-β on Cognitive Decline After Stroke/Transient Ischemic Attack

Plasma homocysteine, apolipoprotein E status and vascular disease in elderly patients with mental illness

Ischemia signalling to Alzheimer-related genes

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