Removal of blood amyloid as a therapeutic strategy for alzheimer's disease: The influence of smoking and nicotine

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Accumulation of amyloid β protein (Aβ) in the brain causes cognitive impairment in Alzheimer's disease (AD). The nature of the relationship between smoking and AD or dementia has been controversial. However, a recent meta-analysis revealed that smoking is a risk factor for AD. With regard to nicotinic acetylcholinergic receptors (nAChRs), both AD and control patients that smoke have been reported to show an increase in 3H-cytisine (an a4β4 nAChR agonist) binding in the temporal cortex. The α7 nAChR is also a key factor in AD pathology, particularly in relation to internalization of Aβs. Furthermore, there are many reports showing the neuroprotective effects of nicotine. The internalization of Aβ may lead to Aβ clearance in the brain. We hypothesized that an extracorporeal system that rapidly removes Aβ from the blood may accelerate Aβ clearance from the brain. We have reported that (1) several medical materials including hemodialyzers can effectively remove blood Aβ, (2) the concentrations of blood Aβs decreased during hemodialysis, (3) removal of blood Aβ enhanced Aβ influx into the blood (ideally from the brain), resulting in maintenance or improvement of cognitive function, and (4) Aβ deposition in the brain of hemodialysis patients was significantly lower than in controls. Smoking affected blood Aβ removal efficiencies and brain atrophy. We believe this Extracorporeal Blood Aβ Removal Systems (E-BARS) may contribute as a therapy for AD.

Original languageEnglish
Title of host publicationNicotinic Acetylcholine Receptor Signaling in Neuroprotection
PublisherSpringer Singapore
Pages173-191
Number of pages19
ISBN (Electronic)9789811084881
ISBN (Print)9789811084874
DOIs
Publication statusPublished - 04-04-2018

Fingerprint

Nicotine
Amyloid
Alzheimer Disease
Smoking
Brain
Therapeutics
Renal Dialysis
Artificial Kidneys
Serum Amyloid A Protein
Nicotinic Receptors
Neuroprotective Agents
Temporal Lobe
Smoke
Cognition
Atrophy
Meta-Analysis
Maintenance
Pathology

All Science Journal Classification (ASJC) codes

  • Medicine(all)
  • Neuroscience(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Kitaguchi, N., Kawaguchi, K., & Sakai, K. (2018). Removal of blood amyloid as a therapeutic strategy for alzheimer's disease: The influence of smoking and nicotine. In Nicotinic Acetylcholine Receptor Signaling in Neuroprotection (pp. 173-191). Springer Singapore. https://doi.org/10.1007/978-981-10-8488-1_10
Kitaguchi, Nobuya ; Kawaguchi, Kazunori ; Sakai, Kazuyoshi. / Removal of blood amyloid as a therapeutic strategy for alzheimer's disease : The influence of smoking and nicotine. Nicotinic Acetylcholine Receptor Signaling in Neuroprotection. Springer Singapore, 2018. pp. 173-191
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Removal of blood amyloid as a therapeutic strategy for alzheimer's disease : The influence of smoking and nicotine. / Kitaguchi, Nobuya; Kawaguchi, Kazunori; Sakai, Kazuyoshi.

Nicotinic Acetylcholine Receptor Signaling in Neuroprotection. Springer Singapore, 2018. p. 173-191.

Research output: Chapter in Book/Report/Conference proceedingChapter

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