OBJECTIVE: To assess the association between lifestyle practices (cognitive and physical activity) and β-amyloid deposition, measured with positron emission tomography using carbon 11-labeled Pittsburgh Compound B ([(11)C]PiB), in healthy older individuals. DESIGN: Cross-sectional clinical study. SETTING: Berkeley, California. PARTICIPANTS: Volunteer sample of 65 healthy older individuals (mean age, 76.1 years), 10 patients with Alzheimer disease (AD) (mean age, 74.8 years), and 11 young controls (mean age, 24.5 years) were studied from October 31, 2005, to February 22, 2011. MAIN OUTCOME MEASURES: Cortical [(11)C]PiB average (frontal, parietal, lateral temporal, and cingulate regions) and retrospective, self-report scales assessing participation in cognitive activities (eg, reading, writing, and playing games) and physical exercise. RESULTS: Greater participation in cognitively stimulating activities across the lifespan, but particularly in early and middle life, was associated with reduced [(11)C]PiB uptake (P < .001, accounting for age, sex, and years of education). Older participants in the highest cognitive activity tertile had [(11)C]PiB uptake comparable to young controls, whereas those in the lowest cognitive activity tertile had [(11)C]PiB uptake comparable to patients with AD. Although greater cognitive activity was associated with greater physical exercise, exercise was not associated with [(11)C]PiB uptake. CONCLUSIONS: Individuals with greater early- and middle- life cognitive activity had lower [(11)C]PiB uptake. The tendency to participate in cognitively stimulating activities is likely related to engagement in a variety of lifestyle practices that have been implicated in other studies showing reduced risk of AD-related pathology. We report a direct association between cognitive activity and [(11)C]PiB uptake, suggesting that lifestyle factors found in individuals with high cognitive engagement may prevent or slow deposition of β-amyloid, perhaps influencing the onset and progression of AD.
"In addition, higher cognitive reserve built through long-term engagement in complex cognitive activities may enhance synaptogenesis and neuronal interconnections that are related to brain reserve, potentially reducing the risk for Aβ downstream cascade or postponing clinical deterioration [Landau et al. 2012; Sperling et al. 2014]. "
[Show abstract][Hide abstract] ABSTRACT: Almost three decades after the publication of the first clinical studies with tacrine,
the pharmacological treatment of Alzheimer’s disease (AD) remains a challenge. Randomized
clinical trials have yielded evidence of significant – although modest and transient – benefit
from cholinergic replacement therapy for people diagnosed with AD, and disease modification
with antidementia compounds is still an urgent, unmet need. The natural history of AD is
very long, and its pharmacological treatment must acknowledge different needs according
to the stage of the disease process. Cognitive and functional deterioration evolves gradually
since the onset of clinical symptoms, which may be preceded by several years or perhaps
decades of silent, presymptomatic neurodegeneration. Therefore, the pharmacological
treatment of AD must ideally comprise both a symptomatic effect to preserve or improve
cognition and a disease-modifying effect to tackle the progression of the pathological process.
Primary prevention is the ultimate goal, should these strategies be delivered to patients
with preclinical AD. In this article, we briefly address the pharmaceutical compounds that
are currently used for the symptomatic treatment of AD and discuss the ongoing strategies
designed to modify its natural course.
Therapeutic Advances in Drug Safety 07/2015; 6(4):151-165. DOI:10.1177/2042098615592116
"Dotyczy to nie tylko aktywności umysłowej. Brak aktywności poznawczej jest typowy dla starszych osób bez otępienia, w których mózgach pojawiły się już zmiany typowe dla AD (Landau et al., 2012). Z aktywnością wiąże się również dłuższy okres pracy zawodowej , czyli przejście na emeryturę w późniejszym wieku. "
"Whether cognitive activity could mitigate disease progression has been explored in a cross-sectional study of amyloid burden in healthy elderly subjects. Those subjects with the highest level of cognitive engagement had a significantly lower cortical amyloid burden, measured with 11 C-PiB, than those with lower levels of engagement  "
[Show abstract][Hide abstract] ABSTRACT: In vivo imaging of amyloid burden with positron emission tomography (PET) provides a means for studying the pathophysiology of Alzheimer's and related diseases. Measurement of subtle changes in amyloid burden requires quantitative analysis of image data. Reliable quantitative analysis of amyloid PET scans acquired at multiple sites and over time requires rigorous standardization of acquisition protocols, subject management, tracer administration, image quality control, and image processing and analysis methods. We review critical points in the acquisition and analysis of amyloid PET, identify ways in which technical factors can contribute to measurement variability, and suggest methods for mitigating these sources of noise. Improved quantitative accuracy could reduce the sample size necessary to detect intervention effects when amyloid PET is used as a treatment end point and allow more reliable interpretation of change in amyloid burden and its relationship to clinical course.
Alzheimer's and Dementia 11/2014; 305. DOI:10.1016/j.jalz.2014.09.004 · 12.41 Impact Factor
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