286:, visual, or dentate-rubro-olivary pathways. Lesions to the brain cause pathological changes that can cause anterograde transneuronal degeneration and lead to system degeneration. Brain lesions create structural or transient deafferntation (the interruption or elimination of sensory nerve impulses by injuring or damaging sensory nerve fibers) 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
472:
also be seen in the endoplasmic reticulum and the golgi apparatuses. The most notable effect is the dense packing of neurotubules (neuronal microtubules). In severely affected cells, this packing greatly reduces the intertubular space to no wider than the tubule. In examining the cells, the tubular outline becomes more pronounced. In axons, similar effects can be seen. There is swelling in mitochondria and other membrane bound
48:, 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. Transneuronal degeneration is thought to be linked to a number of diseases, most notably
484:
There are varying degrees of degeneration. In mild degeneration the cytoplasmic areas shrinks and increases in density and mitochondria swell. However, the endomplasmic reticulum and the golgi apparatuses appear unchanged. The nuclear membrane appears intact, but there is some loss in differentiation
290:
because after the period of latency, neuroplastic rearrangement follows deafferentation. This deafferentation creates interruption of complex circuitry, which can lead to transneuronal structural degeneration. Although studies have shown that lesions can lead to transneuronal degeneration, lesions in
295:
might not cause it. There is not much information on how transneuronal degeneration affects the somatic motor system . Anterograde transneuronal degeneration is not likely to happen since motor neurons are often exhibit convergence (receive input from wide variety of afferent systems). Transneuronal
526:
to determine if this degeneration would lead to loss of neurons. 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. The degeneration led to cell shrinkage and cell death, and these symptoms were more
343:
mitochondrial DNA mutations, which are normally associated with mammalian ageing. The respiratory chain-deficient neurons have adverse effect on normal adjacent neurons, inducing death by means of transneuronal degeneration. Transneuronal degeneration in these cases is accelerated during the ageing
722:
Zappoli, R.; Zappoli, F.; Picchiecchio, A.; Chiaramonti, R.; Grazia
Arneodo, M.; Zappoli Thyrion, G. D.; Zerauschek, V. (2002). "Frontal and Parieto-temporal Cortical Ablations and Diaschisis-like effects on auditory neurocognitive potentials evocable from apparently intact ipsilateral association
471:
as well. There is evident shrinkage in the main dendritic shafts. The concentration of free ribosomes increases and there is a noticeable increase in the granular background of the cytoplasm. In the initial parts of the dendrites, mitochondrial swelling and dilation can be seen. This swelling can
312:
Disconnection syndromes, defined as any neurologic disorder caused by an interruption in impulse transmission along cerebral fiber pathways, can cause white matter brain lesions, leading to secondary neuronal loss and transneuronal degeneration. Secondary neuronal loss occurs as a result in areas
566:
Unilateral perforant pathway transection is a method to study how transneuronal degeneration results from denervation in the
Central Nervous System. Studies are still being done to solidify to connection between candidate molecules creating changes in the central nervous system and postleisonal
39:
when a neuron is overstimulated by a neurotransmitter (most commonly glutamate) causing the dysfunction of that neuron (either damaging it or killing it) which drives neighboring neurons into metabolic deficit, resulting in rapid, widespread loss of neurons. This can be either anterograde or
557:
were not directly connected to the olfactory bulb, but were located closer more superficially. This provided them with them hypothesis that olfactory bulb removal results in transneuronal deafferentation as a result of the massive sudden loss of input from the removed brain tissue.
552:
becomes replaced with large clusters of electron dense material. Once the degeneration has advanced far enough, ribosomes begin to disperse throughout the cell. Some cells are then phagocytosed by astrocytes and microglia. This study showed that the most cells affected by the
547:
and see that these cells rapidly degenerate. The first signs of degeneration seen after the removal of the bulb was mitochondrial swelling and then an increase in electron density in the cytoplasm. Nuclear changes are seen later in which chromatin condenses and the
405:
Transneuronal degeneration creates many telling characteristics in affected cells. The cells themselves tend to shrink, which is best seen in cytoplasmic and nuclear shrinkage. The nucleic acid material becomes reorganized and the distinction between
269:
There are several different mechanisms by which transneuronal degeneration can occur. The technical cause of transneuronal degeneration is the death of neurons resulting from the disruption of input from or output to other nearby neurons.
485:
in nuclear material. In more severely affected cells, the separation between the cytoplasm and nucleus diminishes significantly, causing the cytoplasm to become even more dense and have an increase in electron density.
928:
Terao, S., Li, M., Hashizume, Y., Osano, Y., Mitsuma, T., and Sobue, G. (1997). "Upper motor neuron lesions in stroke patients do not induce anterograde transneuronal degeneration in spinal anterior horn cells".
1342:
Bechmann, Ingo, Deller, Thomas, Del Turco, Domenico, and
Rappert, Angelika. (2007). "Structural reorganization of the dentate gyrus following entorhinal denervation: Species differences between rat and mouse".
978:
Yamada, K., Goto, S., Yoshikawa, M., Okamura, A., and Ushio, Y. (1997). "Continuous intraventricular drug infusion for the in vivo study of transneuronal degeneration in the striatonigral system of the rat".
422:
in the cytoplasm due to the increased concentration of cytoplasmic and nucleic contents. This nucleus degeneration occurs in a later stage than the cytoplasmic effects and results in an increase of condensed
807:
Su, J.H., Deng, G., and Cotman, C.W. (1997). "Transneuronal degeneration in the spread of
Alzheimer's disease pathology: immunohistochemical evidence for the transmission of tau hyperphosphorylation".
100:
support from the target. It occurs in presynaptic cells that are sending inputs to injured postsynaptic cells. It is often termed "dying backward." This type of degeneration can be seen in
575:
of control in mice brains resulted in anterograde neuronal degeneration. This resulted in a smaller microglia response in that area when stimulated in comparison to the wild type group.
56:, and researchers recently have been performing experiments with monkeys and rats, monitoring lesions in different parts of the body to study more closely how exactly the process works.
356:
also have respiratory chain deficiency. This also means that transneuronal degeneration could enhance the consequences of patients with degenerative processes like
Alzheimer’s disease (
360:) because of the neuronal damage from lesions already present. Since neurons are linked in trophic units, this transneuronal degeneration can lead to substantial cell death over time.
257:
into metabolic deficit, resulting in cell degeneration and death. If this exocitotoxic process occurs rapidly, it results in a more rapid death of anterior horn cells resulting in
392:. Evidence of retinal ganglion cell loss consistent with retrograde trans-synaptic degeneration has also been demonstrated in-vivo with optical coherence tomography in humans.
84:. It is often termed "dying forward," and is also referred to as trans-synaptic degeneration. Anterograde degeneration can occur at a late stage of brain injury and result in
368:
Removing portions of an animal's brain can be performed to induce transneuronal degeneration. Transneuronal degeneration results after a sudden massive loss of input from the
476:. There is also a marked increase in cytoplasmic granularity and the dense packing of the neurotubules. Despite these alterations, synaptic specializations appear unchanged.
760:"Transneuronal degeneration in substantia nigra pars reticulata following striatal excitotoxic injury in adult rat: time-course, distribution, and morphology of cell death"
1384:
1246:
1143:
1006:
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911:
850:
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Heimer, L. & Kalil, R. (1978). "Rapid transneuronal degeneration and death of cortical neurons following removal of the olfactory bulb in adult rats".
1402:
Dufour, Eric; Terzioglu, MĂĽgen; Sterky, Fredrik
Hansson; Sörensen, Lene; Galter, Dagmar; Olson, Lars; Wilbertz, Johannes; Larsson, Nils-Göran (2008).
868:, Weidenheim, and Karen M. (2009). "Neuropathology of Cockayne syndrome: Evidence for impaired development, premature aging, and neurodegeneration".
518:
Many studies have been done on monkeys and rats to see the development of transneuronal degeneration after damage to various parts of the brain.
1454:
142:. This results in cell death that is non-apoptotic. More studies need to be done; however, it is hypothesized that this can be related to
337:
It has recently been shown that transneuronal degeneration can also be caused after respiratory chain-deficient neurons develop from
1360:
1222:
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changes. Current studies in rats and mice have provided evidence that microglia cells contribute to transneuronal degeneration of
1048:
Devinsky, O. (2005). "The myth of silent cortex and the morbidity of epileptogenic tissue: Implications for temporal lobectomy".
373:
150:
in which there is major striatal neuronal loss followed by considerable loss of neurons in the substantia nigra pars reticulata.
1205:
Boire, D, Herbin, M, Ptito A, and Ptito M. (1996). "Chapter 28 Neural bases of residual vision in hemicorticectomized monkeys".
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and redistributing those proteins from the axon to the dendrites, which begins the breakdown of routing and sorting mechanisms.
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101:
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also gets replaced with a large homogenous cluster of electron dense material. There appears to be an increase in free
1094:
Dufour, E., Terzioglu, M., Sterky, F.H., Sorensen, L., Galter, D., Olson, L., Wilbertz, J., and
Larsson, N.G. (2008).
314:
296:
degeneration of lower motor neurons is not present after upper motor neuron lesions in stroke patients. In addition
389:
385:
636:
Pinching AJ, Powell TP (1971). "Ultrastructural features of transneuronal degeneration in the olfactory system".
258:
108:
is a variable effect of this disease but the loss of these cells in this disease demonstrates the “dying-back” (
72:
Anterograde transneuronal degeneration is degeneration caused by loss of inputs; it occurs when a neuron in the
489:
cells are only affected in severe cases. They fill in the spaces that have been diminished due to the loss or
595:
1303:"Further Observations on Transneuronal Degeneration in the Lateral Geniculate Nucleus of the Macaque Monkey"
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becoming argyrophilic in silver infused preparations. This allows the researchers to view the cells under
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The reorganization of cellular structures that results from transneuronal degeneration can be seen in
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do not appear to be affected, but there is an appearance of large, empty vacuoles in the cytoplasm.
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all appear to swell, though this can be best seen in the mitochondria which appear to swell first.
344:
process since other cellular maintenance systems are already damaged as well as in the presence of
322:
64:
Transneuronal degeneration can be grouped into two general categories: anterograde and retrograde.
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40:
retrograde, indicating the direction of the degeneration relative to the original site of damage (
1378:
1262:"Retrograde trans-synaptic retinal ganglion cell loss identified by optical coherence tomography"
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creates transneuronal degeneration. A study was done performing enucleation of the eye on
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The
Dentate Gyrus: A Comprehensive Guide to Structure, Function, and Clinical Implications
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28:
24:
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Anterograde and retrograde transneuronal degeneration is typically seen in humans around
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1404:"Age-associated mosaic respiratory chain deficiency causes trans-neuronal degeneration"
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1096:"Age-associated mosaic respiratory chain deficiency causes trans-neuronal degeneration"
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lesions also cause transneuronal degeneration, the effects of which can be seen in the
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36:
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that affected mainly the foveal rim. This also resulted in reduction in the number of
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results from a mutation in genes that interfere with transcription-coupled repair of
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that are strongly connected with the severed tracts or restricted cortex during an
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Extrageniculostriate
Mechanisms Underlying Visually-Guided Orientation Behavior
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Eisen A, Weber M (2001). "The Motor Cortex and
Amyotrophic Lateral Sclerosis".
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and causes them to have dystrophic dendrites. Loss of sensory receptors in the
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162:. It is hypothesized that anterograde transneuronal degeneration causes the
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44:). There are varying causes for transneuronal degeneration such as brain
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Retrograde transneuronal degeneration is degeneration caused by loss of
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of adult rats, anterograde transneuronal degeneration occurs in the
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1347:. Progress in Brain Research. Vol. 163. pp. 501–528.
1209:. Progress in Brain Research. Vol. 112. pp. 385–404.
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cells digest the decaying organelles and dying neurons through
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in monkeys caused retrograde transneuronal degeneration of the
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lesions do not cause anterograde transneuronal degeneration of
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profound after one year than during the first four months.
562:
Unilateral perforant pathway transection in rats and mice
253:. The hyperexcitable corticomotoneurons drive anterior
418:often becomes detached. This causes an increase in
125:
539:is removed has resulted in neurons in the primary
535:Another study being done is on rats in which the
126:Huntington's disease and multiple system atrophy
333:Respiratory chain-deficient neuron development
225:degeneration and transneuronal degeneration.
112:) due to the changes in upper motor neurons.
8:
1383:: CS1 maint: multiple names: authors list (
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76:is damaged and causes the degeneration of a
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80:associated with a similar function as the
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725:International Journal of Psychophysiology
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197:. Neuronal death is predominantly in the
571:-positive dendrites. Denervation in the
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758:Stefanis, L. & Burke, R.E. (1996).
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325:, mammillary bodies, and contralateral
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1260:Jindahra P, Petrie A, Plant G (2009).
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998:
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903:
842:
68:Anterograde transneuronal degeneration
723:areas in humans: five case reports".
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439:does not seem to lose any ribosomes.
372:after it was removed. Removal of the
92:Retrograde transneuronal degeneration
7:
870:Mechanisms of Ageing and Development
249:causes anterograde dengeneration of
463:Transneuronal degeneration affects
514:Eye enucleation in macaque monkeys
245:Evidence supports the theory that
14:
23:resulting from the disruption of
348:, where non-neuronal cells like
140:substantia nigra pars reticulata
201:, but this disease also causes
130:A study done shows that after
1:
1353:10.1016/S0079-6123(07)63027-1
1215:10.1016/s0079-6123(08)63344-0
993:10.1016/s1385-299x(97)00013-5
737:10.1016/S0167-8760(01)00197-0
247:amyotrophic lateral sclerosis
241:Amyotrophic lateral sclerosis
102:Amyotrophic lateral sclerosis
777:10.1016/0306-4522(96)00175-3
596:"Transneuronal degeneration"
493:of the dendritic terminals.
1455:Neurodegenerative disorders
1062:10.1016/j.yebeh.2005.07.020
573:entorhinal-hippicampal area
315:anterior temporal lobectomy
1471:
302:spinal anterior horn cells
259:lower motor neuron disease
41:
17:Transneuronal degeneration
943:10.1161/01.str.28.12.2553
882:10.1016/j.mad.2009.07.006
531:Olfactory removal in rats
443:, endoplasmic reticulum,
1408:Human Molecular Genetics
1035:"Disconnection syndrome"
981:Brain Research Protocols
414:becomes diminished. The
1301:Matthews, M.R. (1964).
1050:Epilepsy & Behavior
809:Neurobiology of Disease
480:Degrees of degeneration
358:see associated diseases
153:
148:multiple system atrophy
821:10.1006/nbdi.1997.0164
520:Enucleation of the eye
378:retinal ganglion cells
308:Disconnection syndrome
74:central nervous system
1176:10.1002/cne.901780310
449:multivesicular bodies
437:endoplasmic reticulum
346:mitochondrial disease
1279:10.1093/brain/awp001
864:Dickson, Dennis W.,
545:electron microscopes
459:Dendritic and axonal
390:magnocellular layers
298:cortico spinal tract
293:somatic motor system
164:hyperphosphorylation
144:Huntington's disease
50:Huntington's disease
650:10.1242/jcs.8.1.253
160:Alzheimer's disease
154:Alzheimer's disease
121:Associated diseases
78:postsynaptic neuron
54:Alzheimer's disease
37:excitotoxic process
1420:10.1093/hmg/ddn030
1112:10.1093/hmg/ddn030
678:Muscle & Nerve
251:corticomotoneurons
82:presynaptic neuron
35:. It is an active
1106:(10): 1418–1426.
1021:"Deafferentation"
937:(12): 2553–2556.
427:aggregation. The
187:mitochondrial DNA
179:Cockayne syndrome
174:Cockayne syndrome
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610:"Excitotoxicity"
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1396:Further reading
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237:are killed.
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116:Presentation
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638:J. Cell Sci
569:parvalbumin
350:glial cells
191:replication
168:tau protein
132:excitotoxic
104:. Loss of
579:References
495:Astrocytes
474:organelles
354:astrocytes
327:cerebellum
255:horn cells
221:result in
215:vestibules
199:cerebellum
110:axonopathy
106:Betz cells
86:diaschisis
1379:cite book
1241:cite book
550:nucleolus
499:microglia
487:Neuroglia
465:dendrites
453:Lysosomes
433:ribosomes
429:nucleolus
425:chromatin
412:cytoplasm
364:Lobectomy
203:apoptosis
42:see types
1449:Category
1438:18245781
1371:17765735
1329:14157007
1288:19224900
1192:32259188
1130:18245781
1078:41726022
1070:16198151
898:34810949
890:19647012
837:29815552
794:25057851
745:11909646
706:24722823
698:11268031
555:necrosis
509:Research
401:Cellular
223:ganglion
136:striatum
27:from or
1429:2367695
1320:1261280
1307:J. Anat
1233:8979844
1121:2367695
951:9412648
829:9440125
786:8895868
658:4101588
491:atrophy
408:nucleus
384:in the
382:neurons
340:de novo
282:in the
280:lesions
274:Lesions
211:cochlea
183:nuclear
166:of the
98:trophic
46:lesions
33:neurons
19:is the
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323:fornix
284:limbic
265:Causes
219:retina
217:, and
193:, and
29:output
1266:Brain
1188:S2CID
1074:S2CID
894:S2CID
833:S2CID
790:S2CID
702:S2CID
469:axons
60:Types
25:input
1434:PMID
1385:link
1367:PMID
1357:ISBN
1325:PMID
1284:PMID
1247:link
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1219:ISBN
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1007:link
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694:PMID
654:PMID
497:and
467:and
447:and
410:and
388:and
352:and
291:the
233:and
185:and
146:and
52:and
1424:PMC
1416:doi
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