TY - JOUR
T1 - Axonal and transneuronal transport in the transmission of neurological disease
T2 - Potential role in system degenerations, including alzheimer's disease
AU - Saper, C. B.
AU - Wainer, B. H.
AU - German, D. C.
N1 - Funding Information:
Acknowledgemenu-Experimentawl ork leading to the ideas expressedin this review was supportedi n part by NINCDS grant NS22835,N S17661,a nd NS20030,b y a Grant-in-Aid from the AmericanH eartA ssociation8 50894, and by grants from the Illinois Departmento f Public Health, the Dallas Area Parkinson’sD iseaseS ociety,t he GreaterD allasA DRDA, theA radineS . Ard Fund, theL ou and Ellen Mcginley Lectureshipa nd the Brain Research Foundation. C.B.S. and B.H.W. were recipients of McKnight ScholarA wards.
PY - 1987/11
Y1 - 1987/11
N2 - Neurons depend upon the processes of axonal and transneuronal transport for intra- and intercellular communication and trophic support. Experimental studies in the last decade have elucidated the mechanisms underlying these processes, and provided evidence for their role in the spread of viral and toxic diseases through the nervous system. Recent advances in neuroanatomy, and in the pathological study of certain degenerative conditions, such as Alzheimer's disease, suggest that the same principles may underlie the anatomical specificity of cell loss in a variety of system degenerations. In Alzheimer's disease, as well as in olivo-ponto-cerebellar atrophy, progressive supranuclear palsy, amyotrophic lateral sclerosis, primary autonomie failure of the Shy-Drager type, and other system degenerations, the main feature that marks the affected populations of neurons is their anatomical interconnectivity. We consider here the possibility that, in these conditions, the processes of axonal and transneuronal transport may subserve the transmission from neuron to neuron of a toxic or infectious agent, or alternatively that the diseases may result from the failure of normal transport of a trophic agent. This hypothesis not only provides a unifying framework in which to view a variety of seemingly disparate conditions, but also suggests certain approaches to identifying the causative agents.
AB - Neurons depend upon the processes of axonal and transneuronal transport for intra- and intercellular communication and trophic support. Experimental studies in the last decade have elucidated the mechanisms underlying these processes, and provided evidence for their role in the spread of viral and toxic diseases through the nervous system. Recent advances in neuroanatomy, and in the pathological study of certain degenerative conditions, such as Alzheimer's disease, suggest that the same principles may underlie the anatomical specificity of cell loss in a variety of system degenerations. In Alzheimer's disease, as well as in olivo-ponto-cerebellar atrophy, progressive supranuclear palsy, amyotrophic lateral sclerosis, primary autonomie failure of the Shy-Drager type, and other system degenerations, the main feature that marks the affected populations of neurons is their anatomical interconnectivity. We consider here the possibility that, in these conditions, the processes of axonal and transneuronal transport may subserve the transmission from neuron to neuron of a toxic or infectious agent, or alternatively that the diseases may result from the failure of normal transport of a trophic agent. This hypothesis not only provides a unifying framework in which to view a variety of seemingly disparate conditions, but also suggests certain approaches to identifying the causative agents.
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U2 - 10.1016/0306-4522(87)90063-7
DO - 10.1016/0306-4522(87)90063-7
M3 - Article
C2 - 2449630
AN - SCOPUS:0023473468
SN - 0306-4522
VL - 23
SP - 389
EP - 398
JO - Neuroscience
JF - Neuroscience
IS - 2
ER -