Pathological ageing refers to ageing that differs from its normal course (e.g. dementia). There are several symptoms of Parkinson’s disease.

1. Tremor (i.e. resting tremor)
2. Slowness of movement
   This consists of two parts. Bradykinesia refers to slow movements and akinesia refers to the absence of movements.
3. Rigidity
   This refers to the stiffness of muscles.
4. Walking and posture
   This refers to walking with a stoop (i.e. walking hunched forward) and walking slower.

Other common features are micrographia (i.e. small handwriting) (1), difficulties doing two things at the same time (2) and an overactive bladder (3). Diagnosis is done by identifying 3 out of 4 major features. It most likely occurs after the age of 50. Medication includes dopamine medication (1), stem cell transplantation (2) and deep brain stimulation (3).

Parkinson’s disease is caused by a degenerating of dopaminergic neurons in the basal ganglia, specifically, in the substantia nigra.

The motor cortex is inhibited due to changes in the basal ganglia’s functioning as a result of a deficiency in the substantia nigra.  The basal ganglia is highly interconnected with the motor circuit (1), associative circuit (2) and limbic circuit (3). There are deficiencies in all areas as a result of Parkinson’s disease.

The direct pathway of the basal ganglia provides inhibitory control over the output structures. The indirect pathway of the basal ganglia excites basal ganglia output structures. This means that the inhibition is increased (i.e. direct pathway decreases inhibition and indirect pathway increased inhibition).

Inhibitory action control refers to a facet of executive cognition that refers to the mechanism or set of processes engaged to suppress behaviours when such actions are reflex-like (1), impulsive (2), inappropriate (3), premature (4), incorrect (5) or no longer relevant (6).

This can be measured using the stop task. This task measures how fast someone can inhibit a voluntary action to a stop signal. It measures the stop-signal reaction time.  The race model states that the winning process (i.e. response process or inhibition process) determines the behaviour. The response process has a U-shaped curve (i.e. slow at childhood, faster during adolescence and adulthood and slower at old age again). There is a less pronounced age development when it comes to the inhibition process.

People with Parkinson’s disease are not slower to respond. However, people with Parkinson’s disease are significantly slower when inhibiting the response.

The stop-change task includes a stop-change signal. This requires a person to reprogram their action when a stop-change signal occurs (e.g. press left instead of right). People with Parkinson’s disease are also significantly slower to change their response compared to healthy controls. The people with Parkinson’s disease show prolonged stopping latencies. It causes a deficit when changing actions.

The subthalamic nucleus, the global pallidus and the inferior frontal gyrus are active when healthy participants are inhibiting a response. The subthalamic nucleus (i.e. a nucleus in the basal ganglia) is a target for deep-brain stimulation as a treatment for Parkinson’s disease. It makes use of a high-frequency currency. This can alleviate motor symptoms. Deep brain stimulation improves response selection and inhibition. It ameliorates the stopping deficit.

The Simon task measures how well a person can inhibit an involuntary action impulse that conflicts with goal-directed behaviour (e.g. Stroop task). This is about selective suppression whereas the stop-task is about inhibiting all responses. In other words, the Simon task requires a person to suppress a motor impulse that is triggered by irrelevant information that conflicts with goal-directed behaviour.

Corresponding trials (C) are characterized by facilitation. There is a faster reaction time and few errors. Non-corresponding trials (NC) are characterized by interference. There is a slower reaction time and more errors.

People respond faster to corresponding trials than to non-corresponding trials during the Simon task. The Simon effect (NC – C) refers to the difference between these two trials (i.e. corresponding and non-corresponding). It is the extra cost and time to solve the interference. Interference control mechanisms may be adjusted proactively between trials (i.e. Simon effect reduces following trials with response conflict). It appears as if people use proactive control after a non-corresponding trial.

The activation-suppression model states that there is automatic response activation but there is deliberate inhibition when the automatic response is incorrect. It holds that the action impulses are rapidly activated by the stimulus location. Strong impulses escape the inhibition and this produces fast errors. A stronger impulse activation leads to a higher percentage of fast errors. People tend to make many fast errors when there is conflict.

The suppression of action impulses takes time to build up within a conflict trial. Therefore, suppression becomes more effective as reaction time slows. This means that more proficient suppression equals a greater reduction of interference as reaction time slows (i.e. when people are slower, the suppression is better and there is less interference). Parkinson’s disease patients are less proficient at suppressing the interference arising from incorrect response capture. There is a dysfunction in inhibitory control processes that operate during action selection.

There is no clear difference between the Simon effect on errors between people with Parkinson’s disease and healthy controls. The interference control is very similar. However, people with Parkinson’s disease are unable to resolve the conflict even when they receive more time. This means that with a slower reaction time, the suppression does not become more proficient.

In other words, Parkinson’s disease impairs selective suppression. This means that they are less able to resolve the conflict. However, this is only apparent when time is taken into account. In Parkinson’s disease, there is a reduction in the capacity to suppress automatic capture by conflicting responses and this increases interference during response selection.

The feature integration model states that features of a stimulus and the response to it for each trial are coded into a memory event that can be activated by overlapping features in the subsequent trial. When one or more features of the memory event are present in the next trial, then the memory event is activated and this produces facilitation effects depending on whether the feature and the responses match.

The effects of old age (i.e. senescence) may reflect limitations in somatic maintenance, resulting in the build-up of damage. Factors associated with vascular and metabolic risk (1), inflammation (2), stress (3) and deposition of iron and beta-amyloid (4) accelerate brain ageing. However, continued neuroplasticity helps maintain the viability of neural structures and postpone the onset of cognitive decline. With ageing, there is a pronounced decrease in dopaminergic neuromodulation. Furthermore, old age is associated with differences in smaller volumes of grey and white matter. In addition to that, it is associated with hippocampal shrinkage.

The supply-demand mismatch model of adult cognitive plasticity states that a mismatch between functional supply and experienced environmental demands can be caused by primary changes in demand (1) or functional supply (2). Functional supply refers to structural constraints imposed by the brain on function and performance. Flexibility refers to the capacity to optimize the brain’s performance within this range. A prolonged mismatch pushes a system away from its equilibrium.

The rates of shrinkage are increased by risk factors. There tends to be a general cognitive decline with age rather than a very specific one. Broad heritability of cognitive factors increases from early to late adulthood.

Physical exercise improves brain plasticity, possibly due to the attenuation of vascular and metabolic risk factors. It is possible that plasticity changes are elicited by a mismatch between environmental demands and organismic supply.

Flexibility refers to the capacity for variations in behavioural repertoire that do not require the reorganization of brain structure and connections. Plasticity refers to changes in behaviour that do require reorganization of brain structure and connections. Mismatches need to be prolonged to overcome the sluggishness of plasticity and push the system away from its current dynamic equilibrium.

The brains of older adults are less likely to respond to environmental challenges with a plasticity response due to the metabolic cost (1) and because the older brain has an enormously large behavioural repertoire (2). This means that it is more likely to opt for flexibility rather than plasticity.

Age-related deficits in memory tend to disappear when the retrieval cues are provided by the environment. It is likely that cognition starts to rely more on environmental support with age. Therefore, attempts at promoting successful ageing should be aimed at the physical and social environment of the individual.

There are different mechanisms which are linked to favourable ageing trajectories:

1. Maintenance
   This holds that brains with well-preserved anatomy and neurochemistry are more likely to generate functional activation patterns that resemble those of younger adults.
2. Compensation
   This holds that structural or functional reorganization of the brain may compensate for ageing-induced losses (e.g. compensatory recruitment of the prefrontal cortex to compensate for the decline in another area).
3. Selection (i.e. greater cognitive reserves)
   This holds that being able to execute a task in multiple ways may make the ageing brain more resilient because the individual has a larger pool of available processing routes.