Monozygotic twins with Alzheimer's disease treated with melatonin: Case report

Abstract

Monozygotic twins with Alzheimer's disease of 8 years duration were studied. The onset of the disease differed by about 6 months between twins and was characterized by a primary impairment of memory function. Clinical evaluation at the time of diagnosis indicated a similar cognitive and neuroimaging alteration in both patients, as well as a similar neuropsychologic impairment. A possible genetic origin of the disease was suggested by a similar disease suffered by the mother. Patients were initially treated with vitamin E (800 I.U./day). Starting at approximately the same time (about 3 years ago), they received 50 mg/day thioridazine because of the behavioral and sleep disorder. One of the patients was treated with melatonin (6 mg orally) at bed time daily for 36 months. Evolution of the disease in the melatonin-treated patient indicated a milder impairment of memory function, with substantial improvement of sleep quality and reduction of sundowning. This led to discontinuance (after 3 months) of thioridazine treatment. Present clinical evaluation indicated a difference in functional stage of the disease between the twins (Functional Assessment Tool For Alzheimer's Disease, FAST), with a score of 5 in the twin who received melatonin and of 7b in the twin who did not receive it. Since experimental data on melatonin in animals indicated its antioxidant, antiapoptotic, and beta-amyloid-decreasing activity, the hypothesis that melatonin has a beneficial effect in Alzheimer's disease patients should be considered.

Melatonin: reducing the toxicity and increasing the efficacy of drugs

“…Thus, should at least the older generation receive supplemental melatonin not only to restore youthful levels of this seemingly bene® cial agent, but also to help them resist the onslaught of destructive reactions that accompany the taking of many medications ? It would seem justi® ed to more extensively test these possibilities in clinical trials, especially given that the studies that have been performed have proven to be successful (Lissoni et al 1997(Lissoni et al , 1999a(Lissoni et al , b, 2001Brusco et al 1998Brusco et al , 2000Cohen-Mans® eld et al 2000 ;Fulia et al 2001 ;Gitto et al 2001a ;Herrera et al 2001 ;Shamir et al 2001).…”

La melatonina como un factor promotor de la diferenciación neuronal: implicaciones en el tratamiento de las demencias

“…63 La administración de esta indolamina a sujetos que padecen EA causa una mejoría en los trastornos de los ritmos circadianos [64][65][66] así como una reducción en la disfunción cognitiva. 67 Los estudios preclínicos apoyan este concepto ya que la MEL actúa como un captador de radicales libres y por lo tanto reduce el estrés oxidativo y la apoptosis.…”

Mitochondrial Disorders Therapy: The Utility of Melatonin~!2009-11-18~!2010-01-21~!2010-06-23~!

“…Taken the results together, the authors suggested that melatonin's cognitive benefits could involve its anti-Aβ aggregation, anti-inflammatory, and/or antioxidant properties [181]. In AD patients, melatonin has been able to stabilize cognitive function over a 2-3 year period [180,182]. An additional retrospective study reported that individuals with mild cognitive impairment given melatonin for sleep enhancement also showed significantly better cognitive performance in two widely utilized cognitive assessment tests [183].…”

“…When neuroblastoma cells were incubated with Aβ, more than 80% of the neurons died due to apoptosis, but the presence of melatonin reduced cellular death and DNA damage in a dose-dependent manner [178]. In human platelets, melatonin also protected against Aβ-induced damage [179,180]. Recently, melatonin treatment has been tested in the APP + presenilin-1 double transgenic (Tg) mouse, which is considered a mouse model with characteristics of the neuropathology of AD [181].…”