There are varying causes for transneuronal degeneration such as brain lesions, disconnection syndromes, respiratory chain deficient neuron interaction, and lobectomies.
Although there are different causes, transneuronal degeneration generally results in the same effects (whether they be cellular, dendritic, or axonal) to varying degrees.
[4] A study done shows that after excitotoxic injury to the striatum of adult rats, anterograde transneuronal degeneration occurs in the substantia nigra pars reticulata.
[7] Cockayne syndrome results from a mutation in genes that interfere with transcription-coupled repair of nuclear and mitochondrial DNA, replication, and transcription.
[1] Anterograde and retrograde transneuronal degeneration is typically seen in humans around lesions in the limbic, visual, or dentate-rubro-olivary pathways.
[10] Brain lesions create structural or transient deafferntation (the interruption or elimination of sensory nerve impulses by injuring or damaging sensory nerve fibers)[11] because injury to the area causes a loss of excitatory input to other areas in the brain, causing them to be less responsive to stimuli.
Delayed secondary transneuronal degeneration can also occur at a late stage after brain injury because after the period of latency, neuroplastic rearrangement follows deafferentation.
Anterograde transneuronal degeneration is not likely to happen since motor neurons are often exhibit convergence (receive input from wide variety of afferent systems).
Secondary neuronal loss occurs as a result in areas that are strongly connected with the severed tracts or restricted cortex during an anterior temporal lobectomy.
Temporal lobe lesions also cause transneuronal degeneration, the effects of which can be seen in the fornix, mammillary bodies, and contralateral cerebellum.
[13] It has recently been shown that transneuronal degeneration can also be caused after respiratory chain-deficient neurons develop from de novo mitochondrial DNA mutations, which are normally associated with mammalian ageing.
Since neurons are linked in trophic units, this transneuronal degeneration can lead to substantial cell death over time.
[15] Removal of the left hemisphere in monkeys caused retrograde transneuronal degeneration of the retinal ganglion cells that affected mainly the foveal rim.
[16] Evidence of retinal ganglion cell loss consistent with retrograde trans-synaptic degeneration has also been demonstrated in-vivo with optical coherence tomography in humans.
This nucleus degeneration occurs in a later stage than the cytoplasmic effects and results in an increase of condensed chromatin aggregation.
It was the first experiment done on adult animals to show evidence of loss of neurons after one year, a long survival period for those affected cells.
Nuclear changes are seen later in which chromatin condenses and the nucleolus becomes replaced with large clusters of electron dense material.
This study showed that the most cells affected by the necrosis were not directly connected to the olfactory bulb, but were located closer more superficially.
[15] Unilateral perforant pathway transection is a method to study how transneuronal degeneration results from denervation in the Central Nervous System.
Current studies in rats and mice have provided evidence that microglia cells contribute to transneuronal degeneration of parvalbumin-positive dendrites.