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In the aging brain, the higher burden of mixed encephalopathy is associated with faster motor decline.
paper uses a new method to determine whether brain pathology explains other aspects of motor decline, such as motion variability.
another innovation in this study is that the authors looked at how much exercise decline and its variability were associated with mixed encephalopathy in the same body.
High load of mixed encephalopathy, including AD, loss of black neurons, Louis, large area infarction, atherosclerosis, small arteriosclerosis, and cerebral amyloid vascular disease, is associated with faster movement loss.
some, but not all, of these neuropathology are also associated with the annual rate of motion variability of these same individuals.
these data suggest that neuropathology has different effects on motion decline: some may affect motion decline, but not motion variability, and some may affect both.
further work is needed to clarify the biological basis and molecular mechanisms behind these findings.
: The average 9-year follow-up data of 1,229 elderly deaths were analyzed.
linear mixing effect model shows an average decline in global motion scores of -0.04 units/year (estimated -0.037, S.E.0.0008, p.lt;0.001).
from these same models, we calculate motion variability as in-person variability in which the global exercise score is relative to the decline of a particular person's movement each year.
, the variation of human-specific motion is 0.013 units/year per year (range 6 x 10-5-0.182).
to test the role of brain pathology, the authors added 10 terms of brain pathology, individually or together, to previous models.
In different models, AD pathology, loss of black neurons, Lewy small body, large area infarction, atherosclerosis, fine arteriosclerosis, and cerebral amyloid vascular disease were associated with faster motor decline.
in a single model, AD pathology, loss of black neurons, and large-scale infarction were associated with decreased motor ability.
AD pathology, loss of black neurons, Louis, large-area infarction and atherosclerosis were associated with human-specific annual exercise variability.
For example, an exponential estimate of the motion variability of the absence of black neurons suggests that the presence of loss of black neurons is associated with a 33 percent increase in motion variability compared to individuals without the loss of black neurons.
next, we examined whether the effects of AD pathological indicators were beta-amyloid proteins, tangles, or both.
when we examined individual models, beta-amyloid proteins and tangles were associated with a decrease in motor capacity.
when the term tangled was added to the same model, the association between beta-amyloid and motor decline decreased and was no longer associated with motor decline.
the marginal association between beta-amyloid protein and annual motion variability is also regulated by adding the word tangle to the same model.
therefore, beta amyloid variants were not associated with motor diseases.
, the effects of brain pathology on exercise injury in old age may be underestimated without more detailed exercise esophysics and individual motor performance characteristics.
further work is needed to determine the neural mechanisms and sites of motion variability and the extent to which motion variability and decline are independent and can be subject to different targeted interventions.
Buchman, A.S., Wang, T., Yu, L. et al. Brain pathologies are associated with both the rate and variability of the development motor function in older adults. Acta Neuropathol (2020). Source: MedSci Originals !-- Content Presentation Ends -- !-- To Determine If Login Ends.