Gerontology & Geriatric Research

Adaptation in the Spine as a Result of Aging

Sandra Nisrin^* Laboratory of Neurobiology and Health, Faculty of Sciences, University of Abdelmalek Essaadi, Tetuan, Morocco
^*Correspondence: Sandra Nisrin, Laboratory of Neurobiology and Health, Faculty of Sciences, University of Abdelmalek Essaadi, Tetuan, Morocco, Email:

Received: 10-Dec-2021 Published: 31-Dec-2021, DOI: 10.35248/2167-7182.21.10.587

Opinion

A spinal neurodegenerative process, which encompasses both structural and functional reorganisation at the spine level, is associated with advanced age. Spinal atrophy is the most important morphological change that occurs in the spinal area. This is mostly due to the death of spinal motor neurons as a result of neural cell apoptosis. Furthermore, it appears that the loss of motor neurons is linked to an increase in the number of astrocytes as well as a change in the dendritic networks. A decline in the number and diameter of myelinated and unmyelinated axons in the ventral horns of the spinal cord has also been found in several human investigations. When compared to young adults, aged individuals have a 38 percent decrease in myelinated and unmyelinated fibres. In a similar investigation on old rodents, it was discovered that when compared to young animals, ageing is characterised by a loss of roughly 40% in myelinated and unmyelinated fibres. These writers consistently found decreased axonal density and myelin thickness, as well as significant connective tissue infiltration and an increase in infolded and out-folded myelin loops.

One of the causes of age-related neurodegeneration at the spinal level has been linked to a decrease in insulin-like growth factor-1 endocrine and paracrine production (IGF-1). IGF-1 acts as both a preventative and compensatory mechanism for the loss of spinal motor neurons as people get older. Researchers discovered that IGF-1 is involved in motor neuron death, motor axon myelination, axonal sprouting stimulation, and axon repair. Although the mechanism underlying the lowering of IGF-1 is yet unknown, it appears that the inflammatory response seen in the majority of aged people may have an impact on local IGF-1 production. Grounds discovered that older persons have higher levels of the inflammatory cytokines TNF-a and TNF-b, and found a robust link between the inflammatory response and decreased IGF-1-mediated motor neuron regeneration and axonal repair. In animal studies, the role of IGF-1 in stimulating axonal sprouting has been revealed. A higher quantity of IGF-1 was associated with a stronger ability to reinnervate denervated muscle fibres when motor neurons were lost in a study on young mice. According to the scientists, reinnervation by axonal sprouting can compensate for the loss of nearly half of the original motor neurons.

The age-related decline in nerve conduction velocity has been attributed to the dysfunction of spinal motor neurons, as well as diminished axonal myelination and shorter internodal length. Reductions in the conduction velocity of peripheral efferent and afferent axon action potentials have been recorded frequently. Variations in nerve conduction velocity, as well as motor and sensory responses, are highly correlated with increasing age. The Hoffman (H) reflex has been shown to be a valid method for assessing the efficacy of spinal circuitry function using electromyography (EMG) and nerve stimulation. The effectiveness of Ia sensory afferent axons in activating spinal motor neurons is predominantly indicated by the H-reflex. EMG and nerve stimulation also allow for the study of the motor (M) wave, which assesses the direct activation of peripheral motor axons and, as a result, the size of the motor response.

Impaired modulation of pre- and post-synaptic spinal inhibition appears to be another factor that contributes to spinal circuitry defects in the elderly. According to some researchers, healthy young individuals can improve muscle force by lowering presynaptic inhibition, which leads to increased excitatory afferent input. Earles and colleagues found that during an isometric voluntary contraction of a leg muscle, older participants had less modulation of spinal pre-synaptic inhibition, despite being able to modulate force comparably to younger people. Similarly, older people increased the co-activation of the antagonist muscle rather than modulating the degree of pre-synaptic inhibition of Ia afferents during a wrist extension task, according to the research. This appears to be linked to a decline in spinal afferent input, implying that in order to generate force, the aged rely less on spinal mechanisms and more on supraspinal mechanisms.