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Related Experiment Videos

Selective nicotinic receptor consequences in APP(SWE) transgenic mice.

Ivan Bednar1, David Paterson, Amelia Marutle

  • 1Divisions of Molecular Neuropharmacology, Occupational Therapy and Elderly Care Research (NEUROTEC), S-141 86 Stockholm, Sweden.

Molecular and Cellular Neurosciences
|July 3, 2002
PubMed
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Nicotinic acetylcholine receptors (nAChRs) increased in the brains of APP(SWE) transgenic mice before cognitive decline. This suggests nAChRs may attempt to compensate for amyloid-beta pathology in Alzheimer

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-beta (Abeta) pathology and cognitive deficits.
  • Acetylcholine receptors (AChRs) play crucial roles in learning and memory.
  • Changes in AChR subtypes and acetylcholinesterase (AChE) activity are implicated in AD pathogenesis.

Purpose of the Study:

  • To investigate alterations in nicotinic (nAChRs) and muscarinic (mAChRs) acetylcholine receptors and acetylcholinesterase (AChE) activity in the brains of APP(SWE) transgenic mice.
  • To determine the temporal relationship between these receptor changes, Abeta pathology, and cognitive impairments.

Main Methods:

  • Studied nAChRs, mAChRs, and AChE activity in APP(SWE) transgenic (Tg+) mice and age-matched nontransgenic (Tg-) controls (4-19 months old).

Related Experiment Videos

  • Utilized radioligand binding assays to quantify specific AChR subtypes: alpha7 nAChRs (125I-alpha-bungarotoxin), alpha4beta2 nAChRs ([3H]cytisine), M1 mAChRs ([3H]pirenzepine), and M2 mAChRs ([3H]AFDX 384).

    • Main Results:

    • A significant increase in alpha7 nAChR binding was observed in most brain regions of 4-month-old Tg+ mice, preceding cognitive deficits and Abeta pathology.
    • This enhanced alpha7 nAChR binding persisted in older Tg+ mice (17-19 months).
    • Increased alpha4beta2 nAChR binding was detected in 17-19-month-old Tg+ mice with heavy Abeta pathology.
    • No significant changes in M1 or M2 mAChR binding were found at any age.

    Conclusions:

    • Upregulation of nAChRs, particularly alpha7 and alpha4beta2 subtypes, occurs in the APP(SWE) mouse model of Alzheimer's disease.
    • These nAChR changes likely represent compensatory mechanisms in response to increasing Abeta burden.
    • The findings highlight the potential involvement of cholinergic system alterations in the early stages of AD-like pathology.