Brain size and the compensation of Alzheimer's disease symptoms: A longitudinal cohort study

Guo, Liang-Hao; Alexopoulos, Panagiotis; Wagenpfeil, Stefan; Kurz, Alexander; Perneczky, Robert; Initiative, Alzheimer’s Disease Neuroimaging

doi:10.1016/j.jalz.2012.10.002

Cited by 49 publications

(45 citation statements)

References 39 publications

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“…These limitations notwithstanding, the compensatory mechanisms modulated by educational level were clearly evident in patients with AD, and appeared partially present also in patients with aMCI. Previous studies have supported the theory of a compensatory role of brain reserve in contrast to a neuroprotective role, demonstrating that greater intracranial volume protects against clinical deterioration in spite of AD-related brain atrophy in aMCI [32].…”

Section: Discussionmentioning

confidence: 84%

The Impact of Cognitive Reserve on Brain Functional Connectivity in Alzheimer's Disease

Bozzali

Dowling

Serra

et al. 2015

JAD

106

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One factor believed to impact brain resilience to the pathological damage of Alzheimer's disease (AD) is the so-called "cognitive reserve" (CR). A critical issue that still needs to be fully understood is the mechanism by which environmental enrichment interacts with brain plasticity to determine resilience to AD pathology. Previous work using PET suggests that increased brain connectivity might be at the origin of the compensatory mechanisms implicated in this process. This study aims to further clarify this issue using resting-state functional MRI. Resting-state functional MRI was collected for 11 patients with AD, 18 with mild cognitive impairment (MCI), and 16 healthy controls, and analyzed to isolate the default mode network (DMN). A quantitative score of CR was obtained by combining information about number of years of education and type of schools attended. Consistent with previous reports, education was found to modulate functional connectivity in the posterior cingulate cortex, whose disconnection with the temporal lobes is known to be critical for the conversion from MCI to AD. This effect was highly significant in AD patients, less so in patients with MCI, and absent in healthy subjects. These findings show the potential neural mechanisms underlying the individual's ability to cope with brain damage, although they should be treated with some caution based on small numbers.

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Section: Discussionmentioning

confidence: 84%

The Impact of Cognitive Reserve on Brain Functional Connectivity in Alzheimer's Disease

Bozzali

Dowling

Serra

et al. 2015

JAD

106

View full text Add to dashboard Cite

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“…It is also possible that volumetric loss in the medial temporal lobe seen in LLD may be due to neurotoxic effect of cortisol. Elevated levels of cortisol are typical for some depressive states associated with hyperactivity of the hypothalamic-pituitary-adrenal axis regulation (Guo et al, 2012). Possible brain changes contributing to LLD are quite diverse and include cerebrovascular, AD, and Lewy body pathology, monoaminergic changes, toxic stress, hypercortisolemia, neuroinflammation, and alterations of neurogenesis and neurotrophic factors, particularly lower blood and cerebrospinal fluid levels of brain-derived neurotrophic factor in LLD compared with controls (Enache et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Neuroanatomical correlates of late-life depression and associated cognitive changes

Lebedeva

Borza

Håberg

et al. 2015

Neurobiology of Aging

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“…The results suggest that optimal neural development in the first couple of years provides a buffer against cerebral pathology in late life [31]. Although greater premorbid brain size seems to protect against clinical deterioration in AD related brain atrophy in Mild Cognitive Impairment (MCI), the protective effects of morphologic reserve seem to be limited to early clinical AD [32].…”

Section: Modifiable Risk Factors Life-course Conceptmentioning

confidence: 99%

Alzheimer’s Disease: An Epidemiologic Disaster From Nutritional Perspective

Péter

2017

JNHFS

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and over was 5.1%. The estimated ratio of these two age groups in the 28 EU countries for 2040 is 17.9% and 9.9%, and for 2050 it is projected to be 17. 2% and 10.9%, respectively [3] (Figure 1).Based on the data available, LE during the 20 th century increased by more than 30 years. By the year 2040 more than a quarter of the Europeans will be older than 65 years and one in seven will be at least 75 years of age. More importantly, health expectancy on average is 8-11 years shorter than LE and loss of cognitive functions and increase in dementia are major contributors of disability and disease during these last couple years of life [4,5].Alzheimer's Disease (AD) is the most common cause of dementia in people aged 60 years or older, representing approximately 60-70% of all cases [6].Currently at least 35 million peopleare affected by AD worldwide and this number is expected to quadruple by the year 2050. Although mortality due to HIV, stroke and heart disease decreased between 2000 and 2013 by 52%, 23% and 14%, respectively, death cases related to AD increased by 71% within the same timeframe, making AD the fourth leading cause of death in developed countries [7].The prevalence of AD increases with age, for example the proportion of people with AD in the US in 2015 was estimated as follows: <65 years: 4%; 65-74 years: 15%; 75-84 years: 43%; 85+ years: 38% [7]. Definition of ADAlois Alzheimer identified the first case of AD in a 51 year old woman, whose brain autopsy showed plaques and tangles that characterize AD [8].AD is a degenerative brain disease of unknown origin, usually developing slowly during the late middle age or in old age and worsens with time. AD results in progressive memory loss, impaired thinking, disorientation, changes in personality and mood. These symptoms are leading to profound decline in AbstractAlzheimer disease (AD) is a progressive, multifactorial, untreatable neurodegenerative disease with worldwide increasing incidence and prevalence in the ageing societies. Besides pharmaceutical drug development there is also a need for alternative solutions for both prevention and treatment. The major objective of this article is to summarize the non-modifiable and some modifiable risk factors of AD, including nutrition and diet, and to discuss different aspects of AD prevention. Optimizing the nutritional status of the general population as a preventive measure may provide additional support to therapeutic concepts as they become available. Already several randomized controlled trials demonstrated promising results for certain nutrients to decrease the risk of developing AD and maintaining cognitive performance. Moreover, symptoms of AD such as neuroinflammation, glucose dysregulation, homocysteine accumulation and neuronal loss can be considerably influenced by nutrition. Thus, lifelong optimal supply of essential micro-and macronutrients may contribute to delay the onset of AD. However, currently the scientific evidence regarding the effects of nutrients on AD is incomplete and there are many...

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Brain size and the compensation of Alzheimer's disease symptoms: A longitudinal cohort study

Cited by 49 publications

References 39 publications

The Impact of Cognitive Reserve on Brain Functional Connectivity in Alzheimer's Disease

The Impact of Cognitive Reserve on Brain Functional Connectivity in Alzheimer's Disease

Neuroanatomical correlates of late-life depression and associated cognitive changes

Alzheimer’s Disease: An Epidemiologic Disaster From Nutritional Perspective

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