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

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

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

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

S1 File -

(DOCX)</p

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