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Call for papers for thematic series:

Biological markers of Alzheimer's disease in non-neuronal cells and tissues. What can we learn from it?

Series Editors:

  • Judith Milklossy (Prevention Alzheimer Foundation, Switzerland)
  • Valerie Askanas (USC Neuromuscular Center, USA)
  • W. King. Engel (University of Southern California, USA)
  • Patrick L McGeer (University of British Columbia, Canada)
  • Kurt Jellinger (Institute of Clinical Neurobiology, Austria)
  • Johannes Attems (Newcastle University, UK)

How to submit?

To contribute to this series please submit a manuscript to Acta Neuropathologica Communications, stating that your manuscript is for this series.

Introduction to the series

Amyloid beta (Aβ), which derives from a larger 120 kDa amyloid precursor protein (APP), is an important biological hallmark of Alzheimer’s disease (AD). Microtubule associated protein tau, which is in a hyperphosphorylated state, is another major biological marker along with chronic inflammation.

APP and tau have fundamental regulatory functions and are synthesized by many cells outside the central nervous system (CNS). This strongly suggests that these phylogenetically highly conserved proteins, together with Aβ, may also occur in various other non-neuronal cells and organs. Indeed, APP gene is widely expressed in non-neuronal cells. The mRNAs for APP, BACE, and PS1, as well as for the Aβ metabolizing enzyme neprilysin have been abundantly detected in organs including heart, liver, spleen and kidney. Various non-neuronal cells including pituitary, adrenal, thyroid and cardiac muscle cells produce large amounts of potentially amyloidogenic APP fragments. Human platelets and lymphocytes produce all forms of APP and secrete amyloidogenic Aβ. Aβ has also been detected not only in the ependymal layer and choroid plexus of brain ventricles, but also in various other organs.

Tau protein is important for microtubule assembly and stabilization. In eukaryotic cells microtubules play an important role in several cellular functions, such as motility, intracellular transport, cell division and in cell shape formation and maintenance. Tau protein mRNA and protein expression is not only present in AD, but it occurs in many neurodegenerative disorders in various organs.

Aβ deposition and/or pathological fibrillary lesions showing similar immunohistochemical and ultrastructural properties to tangles and neuropil threads occur in numerous organs and have been shown to be associated with disorders such as human glaucomas, striated muscle disorders and diabetes. It was also shown that as in AD, these pathological Aβ and tau accumulations are associated with local inflammation.

ApoE-4 genotype is not only a strong risk factor for AD but it is also a risk factor for atherosclerosis, heart disease, type 2 diabetes mellitus, chronic inflammation and infection.

These observations showing that the biological hallmarks of AD are not unique to the CNS, initiate us to revisit this emerging field of research. This special issue might contribute to a better understanding of the significance of these biological markers with respect to the pathogenesis of AD and other neurodegenerative and chronic inflammatory disorders.

Suggested topics

Potential topics include, but are not limited to:

  • Occurrence of APP and Aβ in non-neuronal cells and tissues
  • Occurrence of tau and/or ApoE4 in non-neuronal cells and tissues
  • Accumulation of APP and Aβ in other chronic disorders outside CNS
  • Accumulation of tau and or ApoE4 in other chronic disorders outside CNS
  • Chronic inflammatory processes linked with APP, Aβ, tau or ApoE4 genotype in other neurodegenerative and other chronic disorders outside CNS
  • Importance of APP, Aβ, pTau, ApoE4 and inflammation as systemic markers, with respect to the pathogenesis of AD and other chronic inflammatory disorders
  • Chronic infection linked to these markers