Ageing and the Brain: Difference between revisions

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== Physiological Changes to the brain with ageing ==  
== Physiological Changes to the brain with ageing ==  
There are several physiological changes within the brain which are a result of normal ageing. These are often associated with direct changes in function. Cerebral blood flow has been shown to decrease by 27% decline over 70 years of life (Chen et al, 2011). This is a direct consequence of the age-related changes in the cardiovascular system, and may be exacerbated in patients with atherosclerotic occlusion of the carotid arteries.
The blood-brain barrier (BBB) is formed primarily of tight junctions between adjacent endothelial cells within the blood vessels in the brain. Additionally, specialised neuroglial cells called astrocytes wrap around the cerebral vessels, forming a further physical barrier between the blood and neural tissues. The BBB is essential to prevent most pathogens and many toxic materials crossing into the neural networks and pathways of the brain, but its integrity appears to diminish with age. A recent study indicates that, during normal ageing, the BBB is first weakened in the hippocampus, thereby allowing harmful substances and pro-inflammatory mediators to cross into this vital region of learning and memory. This breaching of the BBB may contribute to hippocampal shrinkage, and therefore to cognitive decline (Montagne et al, 2015).
==== Neurotransmitters ====
Ageing is associated with a declining production of many neurotransmitters, including noradrenaline, glutamate, dopamine and serotonin. The decline in dopamine appears to be particularly important: dopamine modulates motor function and the acquisition of new skills, while also acting as one of the brain’s reward chemicals (Mather, 2016). The number of dopamine-producing neurons decreases as part of the normal ageing process, and this can adversely affect the ability to learn from past experiences. Recent studies show that many older people who boosted their levels of dopamine by taking L-DOPA (a drug normally used to treat Parkinson’s disease) were learning as quickly as young adults again (Chowdhury et al, 2013).


Less resilient and more rigid in outlook, more self-centred, withdrawn and introverted. Learning ability may be impaired and slower. Repeat instructions and supplement them with an exercise sheet or visual prompts and instructions. The number of new exercises may have to be limited and more time allowed learning them, with ample practice, as short-term memory may be shorter.
Less resilient and more rigid in outlook, more self-centred, withdrawn and introverted. Learning ability may be impaired and slower. Repeat instructions and supplement them with an exercise sheet or visual prompts and instructions. The number of new exercises may have to be limited and more time allowed learning them, with ample practice, as short-term memory may be shorter.

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Introduction[edit | edit source]

Ageing refers to the changes that occur in the human body from the attainment of adulthood and ending in death. These changes often involve a decline of biological function and are accompanied by psychological, behavioural, and other changes. Some of these changes are quite obvious, while others are subtle.[1]

Morphological changes to the brain with ageing[edit | edit source]

There are many specific effects of ageing on the brain, although it has been found that these changes are not uniform [2]. It is considered that the volume of the brain is one of the more prominent changes due to neuronal loss, with an approximate reduction of 5% of brain weight, per decade, after the age of 40 [3] Although the changes in diminished intellectual responsiveness, perception, mental agility and efficiency, impaired memory and learning ability are well-known, it is likely that the overall loss of cognition is not a result of widespread neuronal loss, but more small, specific areas affected [2], Additionally, the changes in brain volume have been purported to be a result of changes in white matter and degradation of the myelin as opposed to a reduction of the number of neurones present [4]. Due to the changes in the mass of the neurons alongside others, the brain appears visibly different. Deposition of Brown (Lipofuscin) [5] or black (Neuromelanin)[6] pigments in the brain results in small discoloured areas due to normal ageing, although these are noted more in age-related brain pathologies such as Alzheimer's [7]. In addition to these changes, the neuronal loss makes structures more pronounced such as the sulci of the cortex becoming deeper and the ventricles also becoming more pronounced [7]

Physiological Changes to the brain with ageing[edit | edit source]

There are several physiological changes within the brain which are a result of normal ageing. These are often associated with direct changes in function. Cerebral blood flow has been shown to decrease by 27% decline over 70 years of life (Chen et al, 2011). This is a direct consequence of the age-related changes in the cardiovascular system, and may be exacerbated in patients with atherosclerotic occlusion of the carotid arteries.

The blood-brain barrier (BBB) is formed primarily of tight junctions between adjacent endothelial cells within the blood vessels in the brain. Additionally, specialised neuroglial cells called astrocytes wrap around the cerebral vessels, forming a further physical barrier between the blood and neural tissues. The BBB is essential to prevent most pathogens and many toxic materials crossing into the neural networks and pathways of the brain, but its integrity appears to diminish with age. A recent study indicates that, during normal ageing, the BBB is first weakened in the hippocampus, thereby allowing harmful substances and pro-inflammatory mediators to cross into this vital region of learning and memory. This breaching of the BBB may contribute to hippocampal shrinkage, and therefore to cognitive decline (Montagne et al, 2015).

Neurotransmitters[edit | edit source]

Ageing is associated with a declining production of many neurotransmitters, including noradrenaline, glutamate, dopamine and serotonin. The decline in dopamine appears to be particularly important: dopamine modulates motor function and the acquisition of new skills, while also acting as one of the brain’s reward chemicals (Mather, 2016). The number of dopamine-producing neurons decreases as part of the normal ageing process, and this can adversely affect the ability to learn from past experiences. Recent studies show that many older people who boosted their levels of dopamine by taking L-DOPA (a drug normally used to treat Parkinson’s disease) were learning as quickly as young adults again (Chowdhury et al, 2013).

Less resilient and more rigid in outlook, more self-centred, withdrawn and introverted. Learning ability may be impaired and slower. Repeat instructions and supplement them with an exercise sheet or visual prompts and instructions. The number of new exercises may have to be limited and more time allowed learning them, with ample practice, as short-term memory may be shorter.

Conditions as TIAs, strokes and tonal changes may cause increased anxiety or fear, especially if the person’s balance is affected; falls and low mood can be an issue. Be patient, yet firm. Initially provide more support and encouragement, acting to motivate. Visual impairment will add to the problem.

Reduced intellectual reserves predispose to acute confusional states. Sustained mental, behavioural and motor changes of dementia may include depression (in 10–15% over 65s), persecutory symptoms of paraphrenia plus defective appreciation or localisation of pain. If the individual has an element of low mood, depression or dementia, motivation and participation may be a problem. The person or/and carer may need added emotional support plus teach the carer manual handling or specific exercise regimes. Counselling may form a large part of your role. Conditions such as acute confusion may be a result of dehydration, infection or a stroke, especially if the individual is nil by mouth, so encourage fluid as appropriate. As the therapist, you will need to be aware of mood swings, and if the patient has a tendency to verbal or physical aggression, this will affect your manual handling and their understanding. Remember to assess the risk to yourself first in these cases, especially if working alone.

Macroscopic changes include meningeal thickening, cerebral atrophy (brain weight down 10% between ages 30 and 70, and 20% by 90). Histological changes include: Deposits of lipofuscin in all cells, loss of RNA, mitochondria, enzymes in cytoplasm, decline in function and death of cell in neurones. Neurofibrillary tangles and senile plaques occur. Decrease in neurotransmitters can cause imbalance Vascular changes include fibrosis and degeneration, atheroma that increases in extent with age, but pathogenesis is multifactorial. Transient ischaemic cerebral episodes may progress to a complete stroke. Although different degenerative changes occur with increasing frequency in people over 60, they have not been shown to be directly related with each other.

Sleep pattern shortens, is lighter and more broken, with greater difficulty getting back to sleep again. Worst patterns are found in dementia where confusion increases in the evening or night (sundowning). Impaired sleeping patterns will affect the overall ability to concentrate and participate. Fatigue will also be an issue, so try and find the optimal treatment time.

Sensorimotor performance is slower to achieve accuracy plus impaired sensory awareness to pain, touch, heat, cold and joint position sense. Impaired mechanism controlling posture, antigravity support, balance and moving equipoise (with nerve conduction velocity reduced 10% by the age of 75). Can be a major predisposition to falls and injury.


Resources[edit | edit source]

Ageing and the Central Nervous System: Brain and Spinal cord

References[edit | edit source]

  1. https://www.britannica.com/EBchecked/topic/1354293/human-aging
  2. 2.0 2.1 Burke SN, Barnes CA. Neural plasticity in the ageing brain. Nature reviews neuroscience. 2006 Jan;7(1):30-40.
  3. Svennerholm L, Boström K, Jungbjer B. Changes in weight and compositions of major membrane components of human brain during the span of adult human life of Swedes. Acta neuropathologica. 1997 Sep 1;94(4):345-52.
  4. Murphy DG, DeCarli C, Mclntosh AR, Daly E, Mentis MJ, Pietrini P, Szczepanik J, Schapiro MB, Grady CL, Horwitz B, Rapoport SI. Sex differences in human brain morphometry and metabolism: an in vivo quantitative magnetic resonance imaging and positron emission tomography study on the effect of aging. Archives of general psychiatry. 1996 Jul 1;53(7):585-94.
  5. Ottis P, Koppe K, Onisko B, Dynin I, Arzberger T, Kretzschmar H, Requena JR, Silva CJ, Huston JP, Korth C. Human and rat brain lipofuscin proteome. Proteomics. 2012 Aug;12(15-16):2445-54.
  6. Clewett DV, Lee TH, Greening S, Ponzio A, Margalit E, Mather M. Neuromelanin marks the spot: identifying a locus coeruleus biomarker of cognitive reserve in healthy aging. Neurobiology of aging. 2016 Jan 1;37:117-26.
  7. 7.0 7.1 Knight J, Nigam Y. Anatomy and physiology of ageing 5: the nervous system. Nursing times. 2017 Jun 1;113(6):55-8.