Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 54

With age, some neurons are lost, and others shrink.^9‐10 Neurons attempt to compensate for neuronal loss through dendritic proliferation. There are also increases in support structures such as neuroglia. Unlike other systems of the body, new neurons cannot grow to replace lost neurons. However, the large number of neurons in the CNS prevents the recognition of neuronal losses until they reach a certain threshold. Recent computed tomography and magnetic resonance imaging studies have demonstrated selective atrophy with age, as opposed to a general pattern. Lipofuscin accumulation in nerve cells has also been demonstrated.

At the cellular level, there are increases in neuritic plaques (extracellular masses consisting of an amyloid core surrounded by degenerated neurons) and neurofibrillary tangles (abnormal accumulations of tau protein in neuronal cell bodies). The presence of these unique structures in Alzheimer’s disease led to the hypothesis that this condition may be a form of accelerated ageing.

Age‐related changes also occur in the ANS. The basic change involves slowing of functions, along with prolonged recovery time. Therefore, it is not clear whether individuals are more or less easily stimulated by environmental stimuli as they age.¹¹

There is also attenuation of chemical transmission with age. This occurs because the reduced numbers of functional nerve cells may lessen the strength of the message being transmitted. There are declines in the production of neurotransmitters as well as their receptors.¹² In addition, fewer neurons mean neurotransmitters have to traverse larger spaces, which may result in a loss of message coherence.¹³ Important age‐related changes associated with dopamine signalling are shown in Table 2.1. The total effect of ageing on dopaminergic pathways is decreased function. When dopaminergic function decreases in different regions in the brain, either by decreased synthesis and increased catabolism of dopamine or by receptor desensitization, movement integrity, mood, and capacity for learning new information are impaired. As a result, extrapyramidal findings, signs of depressed mood, and impaired episodic memory can be found on physical examination of affected individuals.

Table 2.1 Age‐related changes in dopaminergic synapses.

Parameter	Changes
Presynaptic markers
Tyrosine hydroxylase immunoreactivity time	↓
Tyrosine hydroxylase activity	↓
Dopamine	→ / ↓
Dopamine turnover	→ / ↑
Cold stress‐induced D turnover increase	↓
Reserpine‐induced D turnover increase	↓
D turnover increase induced by training in reaction	↓
Postsynaptic markers
D1 receptor levels	↓ / →
D2 receptor levels	↓
D1 receptor turnover	↓
D2 receptor turnover	↓
Adenylate cyclase activity	↓
Cyclic‐adenosine‐monophosphateinduced phosphorylation	↓
D/cholecystokinin receptor interaction	↓
D2 denervation supersensitivity	↓

D: dopamine

Ageing individuals also experience a decline in vibration and proprioception sensation via the posterior columns of the spinal cord. This may be due to changes in blood circulation in this region, degeneration of peripheral nerve fibres, or axon loss in the dorsal column.^15,16

Cognitive functions should be evaluated by taking separate histories from patients and their relatives. Patients with non‐age‐related pathological memory impairment often report receiving no complaints, while relatives who live with or are in close contact with these patients complain about their memory loss and are often worried about them. There are several commonly used and easy‐to‐use tools for assessing cognition, including the Mini‐Mental Status Examination, Mini‐Cog test and Montreal Cognitive Assessment.^18‐19 Education level should be considered when interpreting the results of these tests.