greater incidence of glaucomatous damage than other musicians, which was related to life hours of playing. The authors speculated that the cumu- lative effects of long-term intermittent IOP eleva- tions during high resistance wind instrument playing might result in glaucomatous damage. Based on the above research findings and Val- salva hypothesis of AD, extensive use of the VM could be suggested as a possible common risk fac- tor for both NTG and AD. The present author, therefore, hypothesises the presence of a subset of NTGs who may exhibit AD-related pathology due to frequent performance of the VM, predis- posing to both disorders. It could be speculated that excessive Valsalva might be causally related to both NTG and AD through hemodynamic altera- tions. In healthy subjects, it has been shown that the pulsatile ocular blood flow is significantly re- duced during Valsalva and is proportional to the elevation of intrathoracic pressure [5]. Addition- ally, Pott et al. [6] found that, particularly in the upright posture, straining against a closed glottis may critically compromise cerebral perfu- sion. Such hemodynamic alterations are in agree- ment with the currently prevailing concept of vascular involvement in the pathogenesis of both glaucoma and AD [7,8]. With regard to AD, epide- miological studies show that practically all risk factors reported thus far have a vascular compo- nent that reduces cerebral perfusion [8]. It should be stressed, however, that it may be possible to hypothesise other common etiologic fac- tors and pathologic mechanisms that might also ex- ist for both NTG and AD, at least in some patients. References [1] Sugiyama T, Utsunomiya K, Ota H, Ogura Y, Narabayashi I, Ikeda T. Comparative study of cerebral blood flow in patients with normal-tension glaucoma and control sub- jects. Am J Ophthalmol 2006;141:394–6. [2] Wostyn P. Can chronic increased intracranial pressure or exposure to repetitive intermittent intracranial pressure elevations raise your risk for Alzheimer’s disease? Med Hypotheses 2004;62:925–30. [3] Krist D, Cursiefen C, Junemann A. Transitory intrathoracic and – abdominal pressure elevation in the history of 64 patients with normal pressure glaucoma. Klin Monatsbl Augenheilkd 2001;218:209–13. [4] Schuman JS, Massicotte EC, Connolly S, Hertzmark E, Mukherji B, Kunen MZ. Increased intraocular pressure and visual field defects in high resistance wind instrument players. Ophthalmology 2000;107:127–33. [5] Lacey B, Rankin SJA. The effect of increased intrathoracic pressure on pulsatile ocular blood flow. Invest Ophthalmol Vis Sci 1997;38:S781. [6] Pott F, van Lieshout JJ, Ide K, Madsen P, Secher NH. Middle cerebral artery blood velocity during a Valsalva maneuver in the standing position. J Appl Physiol 2000;88:1545–50. [7] Flammer J, Orgul S, Costa VP, et al. The impact of ocular blood flow in glaucoma. Prog Retin Eye Res 2002;21:359–93. [8] de la Torre JC. Alzheimer disease as a vascular disorder: nosological evidence. Stroke 2002;33:1152–62. Peter Wostyn 1 Department of Psychiatry, PC Sint-Amandus, Reigerlostraat 10, 8730 Beernem, Belgium Tel.: +32 56 217438; fax: +32 56 206445. E-mail address: wostyn.peter@skynet.be. doi:10.1016/j.mehy.2006.05.012 Targeting cerebral Bcl-2 expression as a potential therapeutic target in autism: Potential usefulness of human recombinant nerve growth factor Dear Editor, A growing body of evidence has clearly indicated that abnormalities in the neuronal apoptotic path- ways may play a significant role in the pathogenesis of autistic spectrum disorder (ASD) [1]. Accord- ingly, a reduced level of expression of the anti- apoptotic protein Bcl-2 has been consistently demonstrated in the frontal, parietal, and cerebel- lar cortices of ASD patients [2–4]. In the light of these findings, it would be tempting to speculate that stimulation of Bcl-2 expression in the central nervous system may be a potential therapeutic tar- get in autism and related neurodevelopment disorders. We propose that such an effect on cerebral Bcl-2 levels could be achieved via administration of human recombinant nerve growth factor (hrNGF). 1 Minister Lefevrelaan 1, 8500 Kortrijk, Belgium. 1256 Correspondence