Influence of short and long chain Amyloid β peptides on the clenbuterol induced β2-adrenoceptor desensitization.

Influence of short and long chain Amyloid β peptides on the clenbuterol induced β2-adrenoceptor desensitization.</p

Fig 4 -

Influence of the Aβ peptides on the clenbuterol induced β2-adrenoceptor desensitization: The desensitization of the β-AR response by clenbuterol, was not influenced by the short chain Aβ peptides (a). However, the long chain Aβpeptides Aβ 10–37, Aβ1–40, and Aβ1–42 prevent the desensitization and exert a permanent stimulation of the β2-AR signal cascade (b).</p

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Functional effect realized via the β2 adrenoceptor by the truncated Aβ peptide Aβ-[PYR]3–43 (n = 5): This effect was blocked by ICI 118.551 (n-4, p˂0.001), yet not by the β1 adrenoceptor antagonist bisoprolol or the α1-adrenergic antagonist urapidil.

Functional effect realized via the β2 adrenoceptor by the truncated Aβ peptide Aβ-[PYR]3–43 (n = 5): This effect was blocked by ICI 118.551 (n-4, p˂0.001), yet not by the β1 adrenoceptor antagonist bisoprolol or the α1-adrenergic antagonist urapidil.</p

Comparison of the activity of the functional β2-adrenoceptor autoantibodies (β2-AAb) of patients with glaucoma (POAG) (n = 12) and Alzheimer’s disease (AD) (n = 11).

Both agonist-like effects were blocked by the β2-adrenoceptor antagonist ICI 118.551 (0.1μM), (p˂ 0.001). The experiments with the AAb of the AD patients were done in the presence of the α1- adrenoceptor antagonist urapidil to block the agAAb against the α1-adrenoceptor that are also present in the sera of AD patients.</p

Fig 3 -

Desensitization of the β2 adrenergic response by the β2-adrenergic agonist clenbuterol (a). This receptor desensitization was missed if the cells were stimulated with the β2-adrenergic AAb prepared from AD patients (b).</p

MR imaging parameters.

<p>MR imaging parameters.</p

Characteristics of patients receiving plasma exchange therapy.

<p>Characteristics of patients receiving plasma exchange therapy.</p

Patients with Gd enhancement of the optic nerve show significant higher visual improvement.

<p>(A) Mean improvement of visual acuity of patients with or without either T2 lesion or Gd enhancement of the optic nerve in orbital MRI. Error bars indicate standard error of the mean. * indicates significant difference with p = 0.04 as determined via Mann-Whitney rank sum test. Improvement of visual acuity was defined as difference between visual acuity before and after adequate treatment. (B) Mean visual acuity of patients with or without T2 lesion or Gd enhancement of the optic nerve in orbital MRI before and after adequate therapy. Error bars indicate standard error of the mean. No significant differences were found between the single groups.</p

Gd enhancement and T2 lesion of the right optic nerve.

<p>Optic nerve MR imaging of a representative patient with ON. (A) Coronar fat-saturated T1-weighted MRI sequences of the intraorbital and (B) canalicular part of the optic nerve after application of 0.1mmol/kg gadolinium. The arrows highlight the Gd enhanced right optic nerve. (C) Signalalteration of the intraorbital and (D) canalicular part of the optic nerve in coronar fat-saturated T2 turbo spin-echo MRI sequences. The arrows highlight the hypertense T2 lesion of the right optic nerve.</p