Article

Memory after silent stroke: hippocampus and infarcts both matter.

Gertrude H. Sergievsky Center, Department of Neurology, Columbia University, New York, NY, USA.
Neurology (impact factor: 8.31). 01/2012; 78(1):38-46. DOI:10.1212/WNL.0b013e31823ed0cc pp.38-46
Source: PubMed

ABSTRACT Memory decline commonly occurs among elderly individuals. This observation is often attributed to early neurodegenerative changes in the hippocampus and related brain regions. However, the contribution of vascular lesions, such as brain infarcts, to hippocampal integrity and age-associated memory decline remains unclear.
We studied 658 elderly participants without dementia from a prospective, community-based study on aging and dementia who received high-resolution structural MRI. Cortical and subcortical infarcts were identified, and hippocampal and relative brain volumes were calculated following standard protocols. Summary scores reflecting performance on tasks of memory, language, processing speed, and visuospatial function were derived from a comprehensive neuropsychological battery. We used multiple regression analyses to relate cortical and subcortical infarcts, hippocampal and relative brain volume, to measures of cognitive performance in domains of memory, language, processing speed, and visuospatial ability.
Presence of brain infarcts was associated with a smaller hippocampus. Smaller hippocampus volume was associated with poorer memory specifically. Brain infarcts were associated with poorer memory and cognitive performance in all other domains, which was independent of hippocampus volume.
Both hippocampal volume and brain infarcts independently contribute to memory performance in elderly individuals without dementia. Given that age-associated neurodegenerative conditions, such as Alzheimer disease, are defined primarily by impairment in memory, these findings have clinical implications for prevention and for identification of pathogenic factors associated with disease symptomatology.

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    Article: Microembolism infarcts lead to delayed changes in affective-like behaviors followed by spatial memory impairment.
    Christina L Nemeth, Mallory S Shurte, Dana M McTigue, Charles B Nemeroff, Gretchen N Neigh
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    ABSTRACT: Microvascular disease is defined by microvascular events including arterial wall thickening, microvascular lesions, and microembolic stroke. Characteristics of microvascular disease are observed in the vast majority of patients presenting with late-life depression, and changes in affective behavior may precede microvascular-associated changes in cognitive decline. The current study used a microsphere injection model to test the hypothesis that microembolism infarcts induce depressive-like behaviors in rodents. Further, the study sought to determine whether microembolism-induced changes in affective-like behavior preceded deficits in spatial memory. Microbeads were injected into the internal carotid artery to generate microembolic lesions and behavior was assessed at either a short recovery (SR) time point (4-6 days post-surgery) or long recovery (LR) time point (14-17 days post-surgery). A separate cohort of rats was used to assess spatial memory in the Barnes Maze at the LR time point and beyond (35 days post-surgery). Microembolism infarcts led to an increase in anxiety- and depressive-like behaviors at the LR, but not the SR, time point as evidenced by reduced time in the center of the open field, reduced consumption of a sucrose solution, increased latency to approach a novel female at 14 days and impaired spatial memory at 33 days. A thorough analysis of histological markers and lesion volume revealed that gross histological damage was not predictive of behavioral outcomes, suggesting that alterations in neuronal function may underlie behavioral deficits. Collectively, these data demonstrate that microembolism infarcts are sufficient to induce changes in affective-like behavior and these changes precede alterations in spatial memory.
    Behavioural brain research 06/2012; 234(2):259-66. · 3.22 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

658 elderly participants
 
age-associated memory decline
 
age-associated neurodegenerative conditions
 
brain infarcts
 
cognitive performance
 
comprehensive neuropsychological battery
 
disease symptomatology
 
elderly individuals
 
hippocampal volume
 
hippocampus volume
 
Memory decline
 
memory performance
 
poorer memory
 
relative brain volume
 
relative brain volumes
 
smaller hippocampus
 
Smaller hippocampus volume
 
standard protocols
 
subcortical infarcts
 
visuospatial function