Maya Ellison
Tissue plasticity is the ability of tissue to modify its connections and functions in response to environmental demands. It is a critical process in learning and adapting to new environments. Tissue plasticity is known to decrease with age, and this decline is thought to contribute to cognitive decline and age-related diseases. Adipose tissue, for example, undergoes significant changes during aging, leading to physiological declines and age-related diseases. Similarly, brain plasticity, or neuroplasticity, is known to decrease with age, impacting cognitive functions such as learning, memory, and executive functions. However, recent studies suggest that brain plasticity may not be a simple linear decline with age, and that older adults retain some degree of plasticity, allowing them to acquire new skills and adapt to environmental changes.
| Characteristics | Values |
|---|---|
| Tissue plasticity | Decreases with age |
| Brain plasticity | Peaks at a young age, then gradually decreases |
| Brain changes | Functional and structural changes, e.g. reduction in cerebral cortex thickness, grey and white matter changes |
| Cognitive functions | Decline in learning, memory, attention, language, and executive functions |
| Motor functions | Decline in motor performance and abilities |
| Neurotransmitters | Decreased GABA levels, reduced neurotransmitter binding potential |
| Synaptic changes | Decreased synaptic receptor density and efficacy |
| Metabolic changes | Changes in cortical and cerebellar metabolism |
| Adipose tissue | Redistribution of deposits, inflammation, impaired insulin sensitivity |
| APSCs | Proliferation and differentiation capacity decline with age |
| Preadipocytes | Slower growth rate and compromised differentiation in older individuals |
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What You'll Learn
Brain plasticity and cognitive decline
Brain plasticity refers to the brain's ability to alter and adapt the functional properties of networks of neurons. It is a lifetime developmental process that continues to play a significant role in older adulthood. The brain exhibits a higher degree of plasticity during development than in adulthood, and it was once thought that brain plasticity peaked in young adulthood and then gradually decreased with age.
However, mounting evidence now suggests that brain plasticity persists throughout life, even though the rate of plasticity may decrease with age. Advancements in medical imaging techniques have provided evidence for the existence of lifelong brain plasticity, with studies showing that practice induces functional and structural brain changes in both young and older adults. For example, older adults can cope with complex random practice contexts that boost their learning potential and skill retention. This indicates that training-induced neuroplasticity is preserved in older adults, despite lower initial GABA levels.
Despite the evidence for lifelong brain plasticity, cognitive and motor performance generally declines with age. This decline is associated with changes in the structure and function of brain regions, including reductions in cerebral cortex thickness, neurotransmitter binding potential, synaptic receptor density, and efficacy. Additionally, the hippocampus and the prefrontal cortex (PFC) are particularly vulnerable to the effects of ageing, leading to deficits in learning, memory, and executive functions. Age-related cognitive decline is also influenced by vascular damage, amyloid deposition, and interactions between blood vessels and neurodegenerative injuries.
However, it is important to note that an inactive lifestyle and cognitive impairments can also contribute to cognitive and motor performance deterioration, independent of biological ageing. Engaging in physical, motor, or intellectual exercises can help prevent functional decline and preserve cognitive functions. Additionally, motor training can strengthen memory and executive functions, and physical exercise, motor practice, and skill learning can improve motor performance and brain fitness through neural plasticity mechanisms.
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Adipose tissue inflammation
Several lines of preclinical and clinical research have confirmed that chronic low-grade inflammation of adipose tissue is mechanistically linked to metabolic disease. Adipose tissue inflammation is initiated and sustained by dysfunctional adipocytes that secrete inflammatory adipokines and by infiltration of bone marrow-derived immune cells that signal via production of cytokines and chemokines. These immune cells include macrophages, dendritic cells, mast cells, neutrophils, B cells, and T cells. Macrophages are the most abundant, constituting up to 40% of all adipose tissue cells in obesity.
The inflammatory phenotype of expanding adipose tissue involves phenotype changes in hypertrophic adipocytes and tissue-resident immune cells. These changes halt the secretion of anti-inflammatory, protective cytokines and initiate the secretion of inflammatory adipokines and cytokines. Adipose tissue inflammation induces insulin resistance through a variety of molecular mechanisms, and chronic inflammation contributes to the development of insulin resistance and type 2 diabetes in obese individuals.
While brain plasticity is often thought to peak at a young age and then gradually decrease with age, recent evidence suggests that lifelong brain plasticity may exist. Older adults can cope with complex random practice contexts that challenge their instantaneous performance but boost their learning potential and skill retention. This reflects training-induced neuroplasticity in older adults. Similarly, new motor and other skills can be acquired at any age, although progress may be slower in older populations.
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Age-related behavioural changes
Tissue plasticity refers to the ability of tissues to modify their structure and function in response to demands or stimuli. Adipose tissue, for instance, undergoes significant changes during aging, leading to physiological declines and age-related diseases. The proliferation and differentiation capacity of adipose-derived stem cells (ASCs) decline with age, impairing the plasticity of adipose tissue and contributing to insulin resistance.
Brain plasticity, or neuroplasticity, is the brain's ability to modify its connections and functions in response to environmental demands and learning. It is generally accepted that brain plasticity peaks at a young age and gradually decreases with advancing age. This decline in neuroplasticity contributes to cognitive decline, including learning, memory, and executive functions. However, recent evidence suggests that brain plasticity may not be a simple linear decline with age, but rather a complex dysregulation of mechanisms. For example, older rats displayed increased sensitivity to specific audio tones, indicating that the brain's ability to adapt is not lost with age but may be dysregulated due to reduced GABA levels.
Despite the general trend of decreasing brain plasticity with age, older adults retain a degree of neuroplasticity. Cognitive training interventions have shown that older adults can exhibit improved neural activity, develop neural scaffolding, and enhance cognitive functions such as working memory capacity. The ability to acquire new motor skills and adapt to complex practice contexts is also preserved in older individuals, although the progress may be slower compared to younger populations.
In summary, age-related behavioural changes are influenced by a complex interplay of factors, including tissue plasticity, brain plasticity, and cognitive abilities. While certain aspects of tissue and brain plasticity decline with age, recent evidence suggests that the ageing brain retains a degree of plasticity, allowing for behavioural adaptations, cognitive improvements, and the acquisition of new skills.
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Motor cortex plasticity
The primary motor cortex (MI) plays a fundamental role in controlling voluntary movements. Research has revealed that the MI cortex is not merely a static motor control structure. Instead, it exhibits considerable plasticity, with neuronal recordings showing plasticity of MI representations and cell properties following pathological, traumatic, and everyday changes. For example, motor-skill learning and cognitive motor actions can induce plastic changes in the cortical map through reorganization of cortical micro-circuitry and alterations in synaptic efficacy.
The plasticity of the motor cortex is particularly evident in the context of motor learning. Animal studies have demonstrated that motor learning leads to long-term potentiation (LTP) in the primary motor cortex (M1). This learning-induced LTP enhances long-term depression (LTD) while temporarily preventing further potentiation. Non-invasive techniques in humans, such as paired-associative stimulation (PAS) and transcranial magnetic stimulation (TMS), have been used to study LTP-like and LTD-like plasticity during motor learning.
Additionally, mental practice and motor imagery have been shown to induce cortical plasticity. Investigations have revealed that imagined and actual movements trigger similar motor representations and share overlapping brain substrates. Motor imagery has been found to increase M1 excitability, indicating that neuroplasticity can be achieved through mental practice. This has important implications for rehabilitation and skill acquisition, as it suggests that physical practice may not be necessary for improving motor performance.
Advances in medical imaging techniques have provided mounting evidence for lifelong brain plasticity. This has significant implications for our understanding of age-related changes and the potential for older adults to acquire new skills. While progress may be slower in older populations, the ability to adapt and learn persists throughout the lifespan. This knowledge highlights the importance of continued learning and adaptability in a dynamic society, promoting prolonged functional independence and quality of life for older adults.
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Neurodegenerative injuries
The phenomenon of neuroplasticity, or the ability of the brain to reorganise and rebuild itself, has been widely observed in both physiological and pathological conditions. Physiological conditions include developmental plasticity, learning and memory, compensatory plasticity, and repair of the adult brain. Pathological conditions include plasticity after injury, removal of brain tumours, strokes, epilepsy, and neurodegenerative diseases. Neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease are characterised by a progressive decline in cognitive and motor functions, respectively, and are associated with impaired synaptic plasticity and neuronal loss.
The interaction of blood vessels and neurodegenerative injuries may influence the cortical and subcortical neural systems. This damage may alter the local field potentials, which can be measured to assess age-related cognitive decline. The decline in cognitive and motor abilities associated with ageing is a precursor to various diseases. An improved understanding of the impact of ageing on cortical functioning may provide further insight into age-related diseases.
Although the progress may be slower in older adults, new motor and other skills can be acquired at any age. This lifelong brain plasticity is critical for the sustained role of older adults in society and for securing prolonged functional independence and quality of life. For example, exercise rehabilitation training in humans with spinal cord injuries (SCIs) can elicit white matter plasticity in the form of increased myelin water content, leading to positive outcomes in functional recovery.
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Frequently asked questions
It depends on the type of tissue. Brain plasticity is thought to peak at a young age and then gradually decrease as one gets older. However, recent studies have shown that older adults can cope with complex random practice contexts that boost their learning potential and skill retention.
Brain plasticity, or neuroplasticity, refers to the brain's ability to modify its connections and function in response to environmental demands. This is an important process in learning.
The ability to generate new neurons and modify connections in the brain declines with age, contributing to cognitive decline. However, the brain's ability to adapt its functional properties does not disappear completely. Research suggests that plasticity is increased but dysregulated in the aged brain due to reduced GABA levels.
Cognitive training can lead to changes in neural activity and increased neural volume, which may improve cognitive function. However, it is difficult to determine whether these changes reflect a fundamental increase in neural capacity or a change in strategy.
