New research shows that keeping active can help to delay the changes of Alzheimer-related brain changes that Tau levels reach a turning point. Could exercise be a key to postpone the cognitive decline?
Study: Associations between moderate to powerful physical activity, P-TAU181 and cognition in healthy older adults with memory complaints: a secondary analysis of the MAPT. Image Credit: Roman Samorskyi / Shutterstock
Published in a recent study in the magazine The Lancet Healthy LifespanResearchers assessed the associations between fosphorylated (p) -tau181 levels, moderate to powerful physical activity (MVPA) and cognition in older adults.
Tau -proteins are abundantly present in neurons, where they regulate and stabilize the activity of microtubuli in axons and contribute to cell signaling. The aggregation of dysfunctional P-TAU181 in the brain is involved in cognitive decline associated with aging and represents a characteristic of the pathology of Alzheimer’s disease (AD).
That is why it is crucial to determine whether and how these accumulations (from P-TAU181) can be prevented via non-pharmaceutical approaches such as physical activity. Cross-sectional analyzes on the associations between TAU levels and physical activity have yielded different results, whereby some studies reveal inverse associations and others who do not report association. Previous studies have largely found no significant effect of MVPA on the accumulation of P-Tau, making this new research particularly important.
About the study
The current study investigated longitudinal and transversal associations between MVPA, P-TAU181 levels and cognition. They used data from the Multidomain Alzheimer’s Preventive Trial (MAPT), who recruited adults without dementia that were ≥70 of memory centers in Monaco and France.
Eligible participants had self -reported memory complaints, restrictions in instrumental activities of daily life or low running speed. However, individuals were excluded if they had a diagnosed dementia state, a mini-mental state exam (MMSE) score among the 24, limitations in basic activities of daily life, or before registration already took omega-3 supplements. This study included MAPT participants with P-TAU181 measurements at the start, three years or both times. They were randomized to receive one of the four interventions: 1) Multidomain intervention Plus placebo, 2) Multidomain intervention plus omega-3 supplementation, 3) Omega-3 supplementation alone, or 4) placebo alone.
The multidomain intervention included cognitive training and counseling about physical activity and nutrition. Blood samples were analyzed in the clinical neurochemia laboratory at Gothenburg University using a simoa-based internal method. Physical activity was assessed at the start, six months and one, two and three years, with the help of the questionnaire of the Minnesota Leisure Time Activities.
Cognition was assessed at these times with the help of the category name test, the figure symbol substitution test, the 10 mm orientation -items and the free and quated selective memory test. A composite cognitive score was calculated from the scores of these (four) tests. Models with mixed effects were used to investigate the associations between MVPA and P-TAU181 levels and to assess the moderating but non-mediating role of P-TAU181 levels between cognition and MVPA.
Findings
A total of 1,679 people registered from 30 May 2008 to 24 February 2011. Of these, 558 people (33%) had P-TAU181 measurements, with a median basic line of 74. Sixty percent of the subjects were female and 32% were male. Furthermore, the MVPA levels were low for 47% of the participants and high for 45%. Forty -one subjects (7%) were inactive. At the start, the median level of MVPA 1,099 metabolic equivalent task (with) minutes per week, and the median P-TAU181 concentration was 8.9 pg/ml (ranging from 0.4 to 31.7 pg/ml).
The median MMSE score at the start was 28. There was no connection between MVPA levels from Baseline MVPA and Baseline P-TAU181. Nevertheless, there was a significant longitudinal association in which a high degree of MVPA was associated with a lower increase in P-TAU181 levels over time. However, this association was only significant when comparing inactive individuals with active individuals. No difference was found between that with low versus high levels of MVPA.
Furthermore, there was no mediation effect of P-TAU181 levels on the association between MVPA and changes in the composite cognitive score. Moreover, there were no effects of MVPA on changes in the composite cognitive score.
In size analyzes, P-TAU181 levels significantly influenced the associations between MVPA and the composite cognitive score. Higher P-TAU181 levels weakened the positive association between MVPA and cognition. In particular, the effect of MVPA was no longer significant when P-TAU181 levels exceeded the 9.36 pg/ml cross-section and 3.5 pg/ml of longitudinal, which suggests that higher Tau costs can reduce or eliminate the benefits for training.
Conclusions
The findings revealed that MVPA was not associated with P-TAU181 levels at the start, but higher MVPA levels were associated with a lower increase in P-TAU181 levels in time. However, these findings contrast with earlier studies, which have found no effect of MVPA on the accumulation of P-Tau. This suggests that long -term tracking, instead of transversal studies, may be necessary to detect these associations.
In addition, weakened higher baseline P-TAU181 levels The positive association between MVPA and cognition. P-TAU181 levels did not mediate the association between MVPA and Cognition.
The limitations of the study include the usefulness of subjective aids for the assessment of physical activities, which are susceptible to response and recall prejudices. Moreover, physical activity of light intensity and sedentary times were not taken into consideration, which could influence the results. MAPT testers received interventions that may have influenced the observed associations. Moreover, the researchers analyzed the Apoe-ε4 status, but had no influence on the results, indicating that the effects of MVPA at P-TAU181 levels and cognition were independent of the risk factors of genetic Alzheimer. Further analyzes are required to confirm these findings.