The brain in the age of old: The hippocampal formation is targeted differentially by diseases of late life

Wu, W. D.; Brickman, Adam M.; Luchsinger, José A.; Ferrazzano, Peter; Pichiule, Paola; Yoshita, Mitsuhiro; Brown, Truman R.; DeCarli, Charles; Barnes, Carol A.; Mayeux, Richard; Vannucci, Susan J.; Small, Scott A.

doi:10.1002/ana.21557

Cited by 153 publications

(126 citation statements)

References 46 publications

(58 reference statements)

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“…Although none of the subjects had infarcts in the hippocampal formation, infarcts elsewhere in the same vascular territory have been reported to be associated with dysfunction of the hippocampus. 16 However, we found no association between infarcts within PCA territory and hippocampal volume (overall model: F ϭ 0.800, p ϭ 0.165, presence of PCA infarct: ␤ ϭ 0.011, p ϭ 0.165).…”

Section: Samplecontrasting

confidence: 64%

“…The CA1 subfield of the hippocampus is most susceptible to ischemia, and infarcts are related to lower blood volume in this region. 16 Thus, it is also possible that infarcts and neurodegenerative disease affect the hippocampal formation in distinct and complementary ways that result in similar clinical phenotypes. 33 Interestingly, the phenotype may be only grossly identical-with prominent memory deficit-but under the surface there appears to be a unique effect of infarcts and hippocampus volume on memory.…”

Section: Samplementioning

confidence: 99%

“…14 The presence of infarcts likely has a negative effect on information flow due to structural disturbance in cortex and white matter, and may also negatively impact hippocampal function or structure due to the fact that the hippocampus is very sensitive to ischemia. 15,16 There are few studies examining the impact of brain infarcts and hippocampal volume simultaneously in relation to memory performance. Thus, it remains unclear whether infarcts and hippocampus atrophy are related, and contribute to memory decline independently.…”

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confidence: 99%

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Memory after silent stroke

Blum¹,

Luchsinger²,

Manly³

et al. 2012

Neurology

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Objective: 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. Methods:We studied 658 elderly participants without dementia from a prospective, communitybased 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.Results: 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. Conclusions: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. Neurology Memory decline is frequent among the elderly and it is most often attributed to dysfunction and atrophy of the hippocampus and related mesial temporal lobe structures.1-3 Subclinical brain infarcts are present in about one-third of older adults, and are associated with a 2-fold risk of dementia and a steeper decline in age-associated cognitive function. 4 -6 However, the effects of subclinical brain infarcts on hippocampal integrity and age-related memory decline are not well understood. Memory deficits have been described following brain infarcts. Cortical infarcts can result in diverse deficits depending on size and location of lesion and can produce cognitive decline in multiple domains, including perceptual speed and memory. 7,8 Subcortical infarcts can result in executive dysfunction, 9 although strategic thalamic or limbic system infarcts can result in memory loss. 10,11 Clinically, it can be difficult to differentiate between cognitive decline due to

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Section: Samplecontrasting

confidence: 64%

Section: Samplementioning

confidence: 99%

mentioning

confidence: 99%

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Memory after silent stroke

Blum¹,

Luchsinger²,

Manly³

et al. 2012

Neurology

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“…Regarding nutrition, some reports indicated a beneficial effect of resveratrol, a natural polyphenol abundant in grapes and red wine on the health (see Baur and Sinclair 2006 for review). On the contrary, high-fat diet reduces neuronal plasticity in hippocampus and accelerates cognitive deficits (Greenwood and Winocur 2005;Wu et al 2008). Furthermore, a number of vegetables, fruits and food containing unsaturated fatty acid like fish have a positive effect on fluid cognition (Falkenstein 2008;Kang et al 2005).…”

Section: General Factors Affecting Cognitive Functions In Agingmentioning

confidence: 99%

Neurocognition of aging in working environments

Gajewski

Falkenstein

2011

ZAF

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Aging is accompanied by changes in sensory, motor and cognitive functions. Particularly, a high status of socalled fluid cognitive functions is crucial for the employability at an older age. This status, which can be assessed by psychometric and neuroimaging methods, depends on a number of factors like physical constitution, nutrition, education and work demands. This paper systematically analyses factors affecting cognitive functions in aging and reviews current neuroscientific findings regarding training induced neuronal plasticity and compensation of cognitive declines in aging. In the second part the relationship between cognitive functions and the type of work will be discussed and the project PFIFF presented as an example for transfer of neuroscientific basic research to an applied context that aimed at ameliorating and evaluating age-and job-related cognitive deficits. The results of the first project period showed that cognitive decline, as revealed in behavior and brain wave data, may be accelerated by long-lasting unchallenging work and, hence, may occur already in middle age. In the second part of PFIFF a 3-month program consisting of a supervised cognitive training was implemented in a group of 120 assembly-line employees. Before and after the training

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“…The higher serum glucose levels that are common in normal aging directly damage hippocampal structures [13], probably because greater amount of water than normal is required by the eukaryotic cell to move the glucose molecule, lessening the availability of water to produce energy by means of dissociation of the water molecule.…”

Section: Aging-related Process and Human Photosynthesismentioning

confidence: 99%