Luna-Muñoz J, Fuentes P, Hernández-Chan N, Martínez-Fong D, Zamudio S, De la Cruz F, Meraz M, Mena R

Language: Spanish
References: 39
Page: 39-45
PDF size: 82.53 Kb.

ABSTRACT

To date, although several risks factors have been defined to be involved in the develpment of Alzheimer’s disease (AD) in the elderly. Its cause remains unknows. Because of this, the treatment of patients afffected by AD has been limited to a small group of drugs whose effects are usually observed at early stages of the clinical deterioration. Nevertheless, none of these drugs have impact in the evolution of the disease, as they cannot delay or control the massive neuronal loss due to the accumulation of neuritic plaques and tangles in the brain. These structures represent dense accumulations of polymers constituted by β amiloid and tau, respectively. In the present work, we reviewed the different pharmacological treatments available to AD patients, including those inhibiting the Acetyl-colinestases, and hormones. The potential effects of some neuroprophic factors are also described. In particular, we emphasize in the use of cerebrolysin, which is composed by a mixture of brain peptides, which has been successfully used in Europe and Asia in the treatment of mild and severe AD cases. Cerebrolisin has proved effects on the evolution of AD and therefore a promising alternative for the the treatment of such a disease. This review also includes a brief description of the bulk of scientifical data based upon in vivo studies evidencing the molecular mechanisms of cerebrolysin effects.

REFERENCES

1. Salud OMdl: Transtornos neurológicos: desafío para la salud pública. Ginebra: WHO press; 2006

2. Qiu C, De Ronchi D, Fratiglioni L. The epidemiology of the dementias: an update. Curr Opin Psychiatry 2007; 20: 380-5.

3. Ruther E, Ritter R, Apecechea M, et al: Efficacy of the peptidergic nootropic drug cerebrolysin in patients with senile dementia of the Alzheimer type (SDAT). Pharmacopsychiatry 1994; 27: 32-40.

4. Arnold SE, Hyman BT, Flory J, et al. The topographical and neuroanatomical distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer’s disease. Cereb Cortex 1991; 1: 103-16.

5. Arriagada PV, Growdon JH, Hedley-Whyte ET, et al. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer’s disease. Neurology 1992; 42: 631-9.

6. Katzman R, Terry R, DeTeresa R, et al. Clinical, pathological, and neurochemical changes in dementia: a subgroup with preserved mental status and numerous neocortical plaques. Ann Neurol 1988; 23: 138-44.

7. Kondo J, Honda T, Mori H, et al. The carboxyl third of tau is tightly bound to paired helical filaments. Neuron 1988; 1: 827-34.

8. Wischik CM, Novak M, Edwards PC, et al: Structural characterization of the core of the paired helical filament of Alzheimer disease. Proc Natl Acad Sci U S A 1988; 85: 4884-8.

9. Mena R, Edwards PC, Harrington CR, et al. Staging the pathological assembly of truncated tau protein into paired helical filaments in Alzheimer’s disease. Acta Neuropathol 1996; 91: 633-41.

10. Mena R, Edwards P, Perez-Olvera O, et al. Monitoring pathological assembly of tau and beta-amyloid proteins in Alzheimer’s disease. Acta Neuropathol 1995; 89: 50-6.

11. Summers WK, Majovski LV, Marsh GM, et al. Oral tetrahydroaminoacridine in long-term treatment of senile dementia, Alzheimer type. N Engl J Med 1986; 315: 1241-5.

12. Klafki HW, Staufenbiel M, Kornhuber J, et al. Therapeutic approaches to Alzheimer’s disease. Brain 2006; 129: 2840-55.

13. McShane R, Areosa Sastre A,Minakaran N: Memantine for dementia. Cochrane Database Syst Rev 2006; CD003154.

14. Parsons CG, Danysz W, Quack G. Memantine is a clinically well tolerated N-methyl-D-aspartate (NMDA) receptor antagonist—a review of preclinical data. Neuropharmacology 1999; 38: 735-67.

15. Sabbagh MN, Galasko D, Koo E, et al. Amyloid-beta and treatment opportunities for Alzheimer’s disease. J Alzheimers Dis 2000; 2: 231-59.

16. Holmes C, Boche D, Wilkinson D, et al: Long-term effects of Abeta42 immunisation in Alzheimer’s disease: follow-up of a randomised, placebo-controlled phase I trial. Lancet 2008; 372: 216-23.

17. Doody RS, Gavrilova SI, Sano M, et al. Effect of dimebon on cognition, activities of daily living, behaviour, and global function in patients with mild-to-moderate Alzheimer’s disease: a randomised, double-blind, placebo-controlled study. Lancet 2008; 372: 207-15.

18. Gandy S: Data presented at International Conference on Alzheimer’s Disease (ICAD). Vienna. 2009.

19. Wischik CMBP, Wischik D, Seng K. Tau aggregation inhibitor therapy with rember arrest disease progession in mild and moderate Alzheimer’s disease over 50 week. Alzheimer’s and Dementia. 2008; 4: 167.

20. Gould E, Woolley CS, Frankfurt M, et al. Gonadal steroids regulate dendritic spine density in hippocampal pyramidal cells in adulthood. J Neurosci 1990; 10: 1286-91.

21. Toran-Allerand CD, Miranda RC, Bentham WD, et al. Estrogen receptors colocalize with low-affinity nerve growth factor receptors in cholinergic neurons of the basal forebrain. Proc Natl Acad Sci U S A 1992; 89: 4668-72.

22. Birge SJ. Is there a role for estrogen replacement therapy in the prevention and treatment of dementia? J Am Geriatr Soc 1996; 44: 865-70.

23. Honjo H, Ogino Y, Naitoh K, et al. In vivo effects by estrone sulfate on the central nervous system-senile dementia (Alzheimer’s type). J Steroid Biochem 1989; 34: 521-5.

24. Pezet S,McMahon SB. Neurotrophins: mediators and modulators of pain. Annu Rev Neurosci 2006; 29: 507-38.

25. Connor B, Dragunow M. The role of neuronal growth factors in neurodegenerative disorders of the human brain. Brain Res Brain Res Rev 1998; 27: 1-39.

26. Chao MV, Rajagopal R, Lee FS. Neurotrophin signalling in health and disease. Clin Sci (Lond) 2006; 110: 167-73.

27. Phelps CH, Gage FH, Growdon JH, et al. Potential use of nerve growth factor to treat Alzheimer’s disease. Neurobiol Aging 1989; 10: 205-207.

28. Zuccato C, Cattaneo E. Role of brain-derived neurotrophic factor in Huntington’s disease. Prog Neurobiol 2007; 81: 294-330.

29. Saarelainen T, Hendolin P, Lucas G, et al. Activation of the TrkB neurotrophin receptor is induced by antidepressant drugs and is required for antidepressant-induced behavioral effects. J Neurosci 2003; 23: 349-57.

30. Rother M, Kittner B, Rudolphi K, et al. HWA 285 (propentofylline)— a new compound for the treatment of both vascular dementia and dementia of the Alzheimer type. Ann N Y Acad Sci 1996; 777: 404-9.

31. Alvarez XA, Cacabelos R, Laredo M, et al. A 24-week, double-blind, placebo-controlled study of three dosages of Cerebrolysin in patients with mild to moderate Alzheimer’s disease. Eur J Neurol 2006; 13: 43-54.

32. Ruether E, Husmann R, Kinzler E, et al. A 28-week, double-blind, placebo-controlled study with Cerebrolysin in patients with mild to moderate Alzheimer’s disease. Int Clin Psychopharmacol 2001; 16: 253-63.

33. Rockenstein E, Torrance M, Mante M, et al. Cerebrolysin decreases amyloid-beta production by regulating amyloid protein precursor maturation in a transgenic model of Alzheimer’s disease. J Neurosci Res 2006; 83: 1252-61.

34. Veinbergs I, Mante M, Mallory M, et al. Neurotrophic effects of Cerebrolysin in animal models of excitotoxicity. J Neural Transm Suppl 2000; 59: 273-80.

35. Rockenstein E, Mante M, Adame A, et al. Effects of cerebrolysin on neurogenesis in an APP transgenic model of Alzheimer’s disease. Acta Neuropathol 2007; 113: 265-75.

36. Ubhi K, Rockenstein E, Doppler E, et al. Neurofibrillary and neurodegenerative pathology in APP-transgenic mice injected with AAV2-mutant TAU: neuroprotective effects of cerebrolysin. Acta Neuropathol 2009; 117: 699-712.

37. Doppler ERE, Moessler H, Mante M, Adame A, Crews L, Masliah E. Neuroprotective effects of cerebrolysin on neurofibrillary pathology in APP-trangenic ,ice that received neuronal gene transfer with AAV2- Tau. Alzheimer’s and dementia 2008; 4: T484.

38. Nagahara AH, Merrill DA, Coppola G, et al. Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer’s disease. Nat Med 2009; 15: 331-7.

39. Wei ZH HQ, Wang H, Su BH, Chen HZ. Meta-analysis: the efficacy of nootropic agent Cerebrolysin in the treatment of Alzheimer’s disease. Meta-analysis: the efficacy of nootropic agent Cerebrolysin in the treatment of Alzheimer’s disease. 2007; 114: 629-34.