This review focuses on the relationship between obesity and aging and how these interact to affect cognitive function. The topics covered are guided by the Scaffolding Theory of Aging and Cognition ...(STAC Park and Reuter-Lorenz. Annu Rev Psychol 2009;60:173-96-a conceptual model designed to relate brain structure and function to one's level of cognitive ability.
The initial literature search was focused on normal aging and was guided by the key words, "aging, cognition, and obesity" in PubMed. In a second search, we added key words related to neuropathology including words "Alzheimer's disease," "vascular dementia," and "mild cognitive impairment."
The data suggest that being overweight or obese in midlife may be more detrimental to subsequent age-related cognitive decline than being overweight or obese at later stages of the life span. These effects are likely mediated by the accelerated effects obesity has on the integrity of neural structures, including both gray and white matter. Further epidemiological studies have provided evidence that obesity in midlife is linked to an increased risk for Alzheimer's disease and vascular dementia, most likely via an increased accumulation of Alzheimer's disease pathology.
Although it is clear that obesity negatively affects cognition, more work is needed to better understand how aging plays a role and how brain structure and brain function might mediate the relationship of obesity and age on cognition. Guided by the STAC and the STAC-R models, we provide a roadmap for future investigations of the role of obesity on cognition across the life span.
In the research reported here, we tested the hypothesis that sustained engagement in learning new skills that activated working memory, episodic memory, and reasoning over a period of 3 months would ...enhance cognitive function in older adults. In three conditions with high cognitive demands, participants learned to quilt, learned digital photography, or engaged in both activities for an average of 16.51 hr a week for 3 months. Results at posttest indicated that episodic memory was enhanced in these productive-engagement conditions relative to receptive-engagement conditions, in which participants either engaged in nonintellectual activities with a social group or performed low-demand cognitive tasks with no social contact. The findings suggest that sustained engagement in cognitively demanding, novel activities enhances memory function in older adulthood, but, somewhat surprisingly, we found limited cognitive benefits of sustained engagement in social activities.
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BFBNIB, NMLJ, NUK, OILJ, PNG, SAZU, UKNU, UL, UM, UPUK
Brain Trauma Imaging Bischof, Gérard N; Cross, Donna J
Journal of Nuclear Medicine,
01/2023, Volume:
64, Issue:
1
Journal Article
Peer reviewed
Open access
Imaging of mild traumatic brain injury (TBI) using conventional techniques such as CT or MRI often results in no specific imaging correlation that would explain cognitive and clinical symptoms. ...Molecular imaging of mild TBI suggests that secondary events after injury can be detected using PET. However, no single specific pattern emerges that can aid in diagnosing the injury or determining the prognosis of the long-term behavioral profiles, indicating the heterogeneous and diffuse nature of TBI. Chronic traumatic encephalopathy, a primary tauopathy, has been shown to be strongly associated with repetitive TBI. In vivo data on the available tau PET tracers, however, have produced mixed results and overall low retention profiles in athletes with a history of repetitive mild TBI. Here, we emphasize that the lack of a mechanistic understanding of chronic TBI has posed a challenge when interpreting the results of molecular imaging biomarkers. We advocate for better target identification, improved analysis techniques such as machine learning or artificial intelligence, and novel tracer development.
We examined functional activation across the adult lifespan in 316 healthy adults aged 20–89years on a judgment task that, across conditions, drew upon both semantic knowledge and ability to modulate ...neural function in response to cognitive challenge. Activation in core regions of the canonical semantic network (e.g., left IFG) were largely age-invariant, consistent with cognitive aging studies that show verbal knowledge is preserved across the lifespan. However, we observed a steady linear increase in activation with age in regions outside the core network, possibly as compensation to maintain function. Under conditions of increased task demands, we observed a stepwise reduction across the lifespan of modulation of activation to increasing task demands in cognitive control regions (frontal, parietal, anterior cingulate), paralleling the neural equivalent of “processing resources” described by cognitive aging theories. Middle-age was characterized by decreased modulation to task-demand in subcortical regions (caudate, nucleus accumbens, thalamus), and very old individuals showed reduced modulation to task difficulty in midbrain/brainstem regions (ventral tegmental, substantia nigra). These novel findings suggest that aging of activation to demand follows a gradient along the dopaminergic/nigrostriatal system, with earliest manifestation in fronto-parietal regions, followed by deficits in subcortical nuclei in middle-age and then to midbrain/brainstem dopaminergic regions in the very old.
•Lifespan sample age 20–89 finds increasing activation with age on semantic judgment.•When processing demands are increased, modulation of activation declines with age.•Modulation decline gradient: higher to lower nigrostriatal regions as age increases.•Modulation decline is stepwise with age: steep drops in middle- and very old ages.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
The development of in vivo imaging of the pathologic hallmark of Alzheimer disease (AD), β-amyloid (Aβ), altered the framing of its pathophysiology and formulation of inclusion criteria for clinical ...trials. Recent evidence suggests that in vivo measures of Aβ deposition below a threshold indicative of Aβ positivity carry critical information on future cognitive decline and accumulation of AD pathology, potentially already at a younger age. Here, we integrate the existing literature on histopathology of Aβ and its convergence and divergence with in vivo Aβ imaging. The evidence presented amounts to a reconceptualization, in which we advocate for a closer look into Aβ accumulation rates in earlier life, the factors that promote accumulation, comparative studies with different markers of Aβ, and longitudinal designs to elucidate when AD pathology rises and how it shifts from benign to malignant stages that ultimately define AD. These efforts open a new window of opportunity for disease-modifying interventions.
Tau-imaging in neurodegeneration Bischof, Gérard N.; Endepols, Heike; van Eimeren, Thilo ...
Methods (San Diego, Calif.),
11/2017, Volume:
130
Journal Article
Peer reviewed
•The background on tau-pathology in neurodegeneration.•Available tau-tracers and their status of validation.•The purpose and interest in tau-imaging.•The obstacles of development and validation of ...tau PET methods.•Potential clinical applications in early and differential diagnosis.•Follow-up and therapy monitoring using tau-imaging methods.
Pathological cerebral aggregations of proteins are suggested to play a crucial role in the development of neurodegenerative disorders. For example, aggregation of the protein ß-amyloid in form of extracellular amyloid-plaques as well as intraneuronal depositions of the protein tau in form of neurofibrillary tangles represent hallmarks of Alzheimer’s disease (AD). Recently, novel tracers for in vivo molecular imaging of tau-aggregates in the brain have been introduced, complementing existing tracers for imaging amyloid-plaques. Available data on these novel tracers indicate that the subject of Tau-PET may be of considerable complexity. On the one hand this refers to the various forms of appearance of tau-pathology in different types of neurodegenerative disorders. On the other hand, a number of hurdles regarding validation of these tracers still need to be overcome with regard to comparability and standardization of the different tracers, observed off-target/non-specific binding and quantitative interpretation of the signal. These issues will have to be clarified before systematic clinical application of this exciting new methodological approach may become possible. Potential applications refer to early detection of neurodegeneration, differential diagnosis between tauopathies and non-tauopathies and specific patient selection and follow-up in therapy trials.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Is it possible to enhance neural and cognitive function with cognitive training techniques? Can we delay age-related decline in cognitive function with interventions and stave off Alzheimer's ...disease? Does an aged brain really have the capacity to change in response to stimulation? In the present paper, we consider the neuroplasticity of the aging brain, that is, the brain's ability to increase capacity in response to sustained experience. We argue that, although there is some neural deterioration that occurs with age, the brain has the capacity to increase neural activity and develop neural scaffolding to regulate cognitive function. We suggest that increase in neural volume in response to cognitive training or experience is a clear indicator of change, but that changes in activation in response to cognitive training may be evidence of strategy change rather than indicative of neural plasticity. We note that the effect of cognitive training is surprisingly durable over time, but that the evidence that training effects transfer to other cognitive domains is relatively limited. We review evidence which suggests that engagement in an environment that requires sustained cognitive effort may facilitate cognitive function.
Although beta-amyloid (Aβ) positivity has shown to be associated with higher risk of progression to Alzheimer's disease (AD) in mild cognitive impairment (MCI), information on the time to conversion ...to manifest dementia cannot be readily deduced from this binary classification. Here, we assessed if regional patterns of Aβ deposition measured with 18F-florbetapir may serve as biomarker for progression risk in Aβ-positive cognitively normal (CN) and MCI patients, including clinical follow-up data and cerebrospinal fluid (CSF) biomarkers. Voxel-wise group comparisons between age and sex-matched Aβ-positive groups (i.e., CN-stables n = 38 vs. CN-to-MCI/AD progressors n = 38, MCI-stables n = 104 versus MCI-to-AD progressors n = 104) revealed higher Aβ burden in precuneus, subcortical, and parietal regions in CN-to-MCI/AD progressors and cingulate, temporal, and frontal regions in MCI-to-AD progressors. Importantly, these regional patterns predicted progression to advanced stages on the AD spectrum in the short and the long-term beyond global Aβ burden and CSF biomarkers. These results suggest that distinct regional patterns of Aβ burden are a valuable biomarker for risk of disease progression in CN and MCI.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Tau aggregation following subcortical hemorrhage Jaeger, Elena; Bischof, Gérard N.; Onur, Oezguer A. ...
European journal of nuclear medicine and molecular imaging,
07/2024, Volume:
51, Issue:
8
Journal Article
Peer reviewed
Open access
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ