Axonal and transneuronal transport in the transmission of neurological disease: Potential role in system degenerations, including alzheimer's disease

Saper, CB; Wainer, Bruce H.; German, Dwight C.

doi:10.1016/0306-4522(87)90063-7

Cited by 220 publications

(113 citation statements)

References 84 publications

Supporting

Mentioning

106

Contrasting

Order By: Relevance

“…The mechanism may be similar to that of transneuronal degeneration proposed to be due to failure of one neuron to transport a trophic agent to another (39). The ligand of the c-Kit receptor, steel factor, can be found in nerves (47), but this cannot be confirmed in all tissues or species (48).…”

Section: Discussionmentioning

confidence: 88%

Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus

Huizinga¹,

Reed²,

Berezin³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

cells of Cajal (ICC) have been proposed as stretch receptors for vagal afferent nerves in the stomach based on immunohistochemical studies. The aim of the present study was to use electron microscopy and the anterograde degeneration technique to investigate ultrastructural features and survival dependency of ICC associated with vagal afferent innervation of the cat esophagus. This is the first report on the ultrastructural characteristics of ICC in the cat esophagus. Intramuscular ICC (ICC-IM) were identified throughout the musculature, whereas ICC in the myenteric plexus were rare. ICC-IM were particularly numerous in septa aligned with smooth muscle bundles. They were in synapse-like contact with nerve varicosities and in gap junction contact with smooth muscle cells. Smooth muscle cells also made contact with ICC through peg and socket junctions. Precision damage through small-volume injection of saline in the center of the nodose ganglion from the lateral side, known to selectively affect sensory nerves, was followed within 24 h by degeneration of a subset of nerve varicosities associated with ICC-IM, as well as degeneration of the associated ICC-IM. Smooth muscle cells were not affected. Nerves of Auerbachs plexus and associated ICC were not affected. In summary, ICC-IM aligning the esophageal muscle bundles form specialized synapse-like contacts with vagal afferent nerves as well as gap junction and peg-and-socket contacts with smooth muscle cells. This is consistent with a role of ICC-IM as stretch receptors associated with vagal afferent nerves; the ICC-vagal nerve interaction appears essential for the survival of the ICC. interstitial cells of Cajal; esophagus; stretch receptor; vagus; afferent innervation; intramuscular interstitial cells of Cajal FOR NORMAL ESOPHAGEAL function, the vagus nerves provide the major sensory and motor innervation to both striated and smooth muscle portions of the esophagus. Sensory pathways from the esophagus have been studied both electrophysiologically (40, 41) and by nerve tracing techniques (4,11,28). However, the precise location and structure of the sensory receptor(s) involved in control of esophageal motor function remain controversial. It is likely that more than one structurally and functionally distinct type of mechanoreceptor exists within the esophagus (4, 5, 8). As early as 1929, intraganglionic laminar nerve endings (IGLE) were considered candidates for esophageal stretch receptors (34). In an elegant study by Berthoud and Powley (4), intramuscular vagal afferents were shown to be positioned and structured as likely candidates for the gastric stretch receptor. Intramuscular arrays (IMA) enter circular or longitudinal muscle layers, run parallel to respective muscle fibers, and bifurcate to create an array of parallel terminal elements in stomach and sphincters (28). In the stomach, these terminal elements consist of interconnected parallel axonal telodendria that are arrayed in close proximity to one another and that form appositions with interstitial cells ...

show abstract

Section: Discussionmentioning

confidence: 88%

Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus

Huizinga¹,

Reed²,

Berezin³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…Key lesions in sporadic PD consist of aggregated forms of a-synuclein, a protein located chiefly in axons and their presynaptic terminals (Eisenberg and Jucker 2012;Jucker and Walker 2013;Kaufman and Diamond 2013;Goedert et al 2014). Notably, all brain regions and all types of nerve cells consecutively involved in AD or PD are anatomically interconnected over considerable distances, thereby indicating that physical contact among such interconnected nerve cells plays a key role in the pathogenesis of both illnesses (Pearson et al 1985;Saper et al 1987;Pearson and Powell 1989;Pearson 1996;Duyckaerts et al 1997;Braak and Del Tredici 2011b). Ab is deposited extracellularly and thus is not known to transfer from one nerve cell to the next in the neuronal chain (Fiala 2007;Kaufman and Diamond 2013).…”

mentioning

confidence: 99%

Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases

Braak

Tredici

2016

Cold Spring Harb Perspect Biol

108

View full text Add to dashboard Cite

Experimental data indicate that transneuronal propagation of abnormal protein aggregates in neurodegenerative proteinopathies, such as sporadic Alzheimer's disease (AD) and Parkinson's disease (PD), is capable of a self-propagating process that leads to a progression of neurodegeneration and accumulation of prion-like particles. The mechanisms by which misfolded tau and a-synuclein possibly spread from one involved nerve cell to the next in the neuronal chain to induce abnormal aggregation are still unknown. Based on findings from studies of human autopsy cases, we review potential pathways and mechanisms related to axonal and transneuronal dissemination of tau (sporadic AD) and a-synuclein (sporadic PD) aggregates between anatomically interconnected regions. S poradic Alzheimer's disease (AD) and Parkinson's disease (PD) are human neurodegenerative disorders that do not occur in other vertebrate species. Pathological hallmark lesions in AD and PD involve only a few types of nerve cells, mainly projection neurons. These lesions develop at predetermined predilection sites and progress according to predictable patterns (Braak and Del Tredici 2009, 2015). In AD, disease-related lesions remain confined to the central nervous system (CNS), whereas in PD they develop not only in the CNS but also in the enteric (ENS) and peripheral (PNS) nervous systems. Both diseases are caused by misfolding of specific proteins that are associated with aberrant aggregation. AD is primarily characterized by pathological forms of the intraneuronal protein tau (Goedert et al. 2006;Iqbal et al. 2009) and, thereafter gradually, by extracellular deposits of the b-amyloid protein (Ab) (Alafuzoff et al. 2009;Haass et al. 2012;Masters and Selkoe 2012). In mature nerve cells, the highest concentrations of the protein tau usually are found in the axon. Key lesions in sporadic PD consist of aggregated forms of a-synuclein, a protein located chiefly in axons and their presynaptic terminals (Eisenberg and Jucker 2012;Jucker and Walker 2013;Kaufman and Diamond 2013;Goedert et al. 2014). Notably, all brain regions and all types of nerve cells consecutively involved in AD or PD are anatomically interconnected over considerable distances, thereby indicating that physical contact among such interconnected nerve cells plays a key role in the pathogenesis of both illnesses (Pearson et al. 1985;Saper et al. 1987;Pearson and Powell 1989;Pearson 1996;Duyckaerts et al. 1997;Braak and Del Tredici 2011b). Ab is deposited extracellularly and thus is not known to transfer from one nerve cell to the next in the neuronal chain (Fiala 2007;Kaufman and Diamond 2013).Here, we focus on potential pathways and mechanisms related to the postulated transmission and transneuronal dissemination of tau and a-synuclein between involved neurons and as yet uninvolved neurons in anatomically connected regions (Brundin et al. 2008Clavaguera et al. 2009Clavaguera et al. , 2013aDesplats et al. 2009;Luk et al. 2009;Angot et al. 2010 Angot et al. , 2012Frost and Diamond 2010;Goedert...

show abstract

“…In addition, TA [82,102,175] are present in the motor cortex and striatum in PSP [51]. Neurons affected in PSP also appear to be functionally related, NFT occurring in interconnected extrapyramidal and oculomotor structures [151]. The presence of astrocytic pathology is regarded as a diagnostic feature of PSP [82] which may distinguish the disorder from the closely related CBD [81,109].…”

Section: Cellsmentioning

confidence: 99%

Can neurodegenerative disease be defined by four ‘primary determinants’: anatomy, cells, molecules, and morphology?

Armstrong

2016

View full text Add to dashboard Cite

A b s t r a c t , the anatomical pathways affected by the disease ('anatomy'), the cell populations affected ('cells'), the molecular pathology of 'signature' pathological lesions ('molecules'), and the morphological types of neurodegeneration ('morphology'). This review first discusses the limitations of existing classificatory systems and second provides evidence that the four primary determinants could be used as axes to define all cases of neurodegenerative disease.To illustrate the methodology, the primary determinants were applied to the study of a group of closely related tauopathy cases and to heterogeneity within frontotemporal lobar degeneration with .

show abstract

Axonal and transneuronal transport in the transmission of neurological disease: Potential role in system degenerations, including alzheimer's disease

Cited by 220 publications

References 84 publications

Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus

Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus

Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases

Can neurodegenerative disease be defined by four ‘primary determinants’: anatomy, cells, molecules, and morphology?

Contact Info

Product

Resources

About