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Decline of functions, malfunctions and atrophy are secondary.
Secondly, objective factors of burden that are related to disease symptoms (e.g. problem behaviours and the decline of functions).
For example, animal model studies (Bahar et al. 2006; Herndon et al. 2002) have reported increased cell-to-cell variation in gene expression with age- and tissue-specific decline of functions associated with stochastic events.
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The hard fact of aging is the body's decline of function: Muscles lose strength and mass, bones become fragile, the heart beats slower, and brain function becomes impaired before death.
mTOR-dependent hyperfunction and hypertrophy of beta-cells, may eventually culminate in cell loss and decline of function [ 177, 178].
A premature invo-lution of the thymus and a decline of function of T cell-dependent immunity is inherent in OXYS rats [ 15, 16].
A decline of function in the neuromuscular junction has long been thought to contribute to the decline of muscle mass with age (Bütikofer et al., 2011).
Within this framework the neurobiological reason for the distinct time course of decline of function is selective vulnerability of brain regions.
The non-linearity of the decline of function impedes the calculation of effect sizes based on cumulative values from these multidimensional scales.
The individual assessment of these dimensions is meant to identify individual risk factors or a decline of functioning, leading to a need for individual intervention strategies.
This could be the result of mechanisms that buffer, adapt, or remodel, leading to only a negligible decline of functioning initially (see e.g. Rattan 2006).
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