FROM: THE FACULTY OF PHARMACY Ph.D. STUDIES IN PHARMACEUTICAL SCIENCE
ALIAmides: EXPERIMENTAL STUDIES ON THE CONTROL OF ANGIOGENESIS
BY: Ph. D. Student: MARIATERESA CIPRIANO
The acronym ALIA (Autacoid Local Inflammation Antagonism) was
formulated when Aloe et al. (1993), when he indicated that some
endogenous N-acylethanolamines exerted a local antagonism on
inflammation (Fig. 2.1.1.).
Rita Levi-Montalcini and co-workers (1996) modified the acronym into
Autacoid Local Injury Antagonism, in order to explain the mechanism of
action of Palmitoylethanolamide (PEA) and related fatty acid amides. This
change was made following the observation that the pharmacological
effects of PEA appear to reflect the consequences of supplying the tissue
with a sufficient quantity of its physiological regulators of cellular
homeostasis (Levi-Montalcini et al., 1996). The effect was first attributed to
mast-cell activity control. Concomitantly, Mazzari et al. (1996) demonstrated
that the in vivo anti-inflammatory effects of PEA were due to downregulation
of mast-cell degranulation.
Similar results have recently been obtained in dogs and cats. In fact,
densitometric analysis performed on skin biopsies from cats with
eosinophilic granuloma complex and treated with PEA, revealed an
increase in the granular density of cutaneous mast-cells, thereby
suggesting a decrease in mast-cell degranulation (Scarampella et al.,
Using similar techniques, an inhibitory control over mast-cell degranulation
has been demonstrated in dogs locally exposed to PEA analogues.
Together with PEA, other compounds acting as ALIAmide has been
described; however, starting from these evidences, Palmitoylethanolamide
is considered as the early ALIAmide.