Int J Clin Exp Hypn. 2008 Jul;56(3):318-33. Links
Hypnotic approaches for alopecia areata.Willemsen R, Vanderlinden J.

Alopecia areata (AA) is an autoimmune disease leading to loss of scalp hairs. The disease seems triggered by stress. Data on the possibility of using hypnotherapy in the treatment of AA are very limited. Twenty-eight patients with extensive AA, all refractory to previous conventional treatment, were treated with hypnosis at the Academic Hospital UZ Brussel, Brussels, Belgium. This paper describes in detail the authors’ hypnotherapeutic approach combining symptom-oriented suggestions with suggestions to improve self-esteem. Twelve out of 21 patients, including 4 with total loss of scalp hair, presented a significant hair growth. All patients presented a significant decrease in scores for anxiety and depression. Although the exact mechanism of hypnotic interventions has not been elucidated, the authors’ results demonstrate that hypnotic interventions may ameliorate the clinical outcome of patients with AA and may improve their psychological well-being.

Nat Med. 2008 Jul;14(7):767-72. Epub 2008 Jun 29.

Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging.

Varela I, et al

Several human progerias, including Hutchinson-Gilford progeria syndrome (HGPS),are caused by the accumulation at the nuclear envelope of farnesylated forms of truncated prelamin A, a protein that is also altered during normal aging. Previous studies in cells from individuals with HGPS have shown that farnesyltransferase inhibitors (FTIs) improve nuclear abnormalities associated
with prelamin A accumulation, suggesting that these compounds could represent a therapeutic approach for this devastating progeroid syndrome. We show herein that both prelamin A and its truncated form progerin/LADelta50 undergo alternative prenylation by geranylgeranyltransferase in the setting of farnesyltransferase
inhibition, which could explain the low efficiency of FTIs in ameliorating the phenotypes of progeroid mouse models. We also show that a combination of statins and aminobisphosphonates efficiently inhibits both farnesylation and geranylgeranylation of progerin and prelamin A and markedly improves the aging-like phenotypes of mice deficient in the metalloproteinase Zmpste24, including growth retardation, loss of weight, lipodystrophy, hair loss and bone
defects. Likewise, the longevity of these mice is substantially extended. These findings open a new therapeutic approach for human progeroid syndromes associated with nuclear-envelope abnormalities.

Prelamin A farnesylation and progeroid syndromes. [J Biol Chem. 2006]

Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes. [Proc Natl Acad Sci U S A. 2005] PMID:16129834

Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. [Proc Natl Acad Sci U S A. 2005] PMID:16014412

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. [Proc Natl Acad Sci U S A. 2005]

A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. [J Clin Invest. 2006]