Loss of intraventricular fluid melatonin can explain the neuropathology of Alzheimer's disease

Maurizi, C.P.

doi:10.1016/s0306-9877(97)90220-6

Cited by 28 publications

(21 citation statements)

References 38 publications

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“…A decrease in the cerebrospinal fluid (CSF) melatonin was found in patients with AD and subsequently it was suggested that the loss of melatonin allowed neuronal mitochondria to be damaged by endogenously-generated S OH, with injury noted first in the most active tissues (Maurizi, 1997(Maurizi, , 2001Cardinali, 2003). In fact, results from initial therapeutic trials of melatonin in AD patients have demonstrated improved function, decreased ''sundowning'', improved sleep, and a significant slowing of the progression of the disease (Maurizi, 2001;Cardinali, 2003).…”

Section: Melatonin Mitochondria and Neurodegenerative Disordersmentioning

confidence: 99%

Melatonin and mitochondrial function

León¹,

Acuña-Castroviejo

Sainz³

et al. 2004

Life Sciences

303

249

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Section: Melatonin Mitochondria and Neurodegenerative Disordersmentioning

confidence: 99%

Melatonin and mitochondrial function

León¹,

Acuña-Castroviejo

Sainz³

et al. 2004

Life Sciences

303

249

View full text Add to dashboard Cite

“…Maurizi stated the hypothesis that the attenuation of the melatonin rhythm could explain the neuropathology of Alzheimer's disease and suggested administration of melatonin (Maurizi, 1997). The aim of this study was to evaluate a possible additional eect of melatonin on motor restless behaviour and sundowning in demented patients treated with bright light.…”

Section: Introductionmentioning

confidence: 99%

Bright light therapy and melatonin in motor restless behaviour in dementia: a placebo-controlled study

Haffmans

Sival

Lucius

et al. 2001

Int. J. Geriat. Psychiatry

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“…Under normal conditions, MT is an immunostimulator, preparing the body to enter a pre-activated state and to eliminate pathogens more effectively [27]. This immunostimulating effect is particularly important under immunosuppressive conditions, such as in Alzheimer′s disease [49,50]. In contrast, MT also exerts negative regulatory effects in situations of exacerbated immune response, such as in sepsis and other autoimmune disorders [24,51,52].…”

Section: Discussionmentioning

confidence: 99%

Responses of Transgenic Melatonin-Enriched Goats on LPS Stimulation and the Proteogenomic Profiles of Their PBMCs

Yang

Tao

et al. 2018

IJMS

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The anti-inflammatory activity of melatonin (MT) has been well documented; however, little is known regarding endogenously occurring MT in this respect, especially for large animals. In the current study, we created a MT-enriched animal model (goats) overexpressing the MT synthetase gene Aanat. The responses of these animals to lipopolysaccharide (LPS) stimulation were systematically studied. It was found that LPS treatment exacerbated the inflammatory response in wild-type (WT) goats and increased their temperature to 40 °C. In addition, their granulocyte counts were also significantly elevated. In contrast, these symptoms were not observed in transgenic goats with LPS treatment. The rescue study with MT injection into WT goats who were treated with LPS confirmed that the protective effects in transgenic goats against LPS were attributed to a high level of endogenously produced MT. The proteomic analysis in the peripheral blood mononuclear cells (PBMCs) isolated from the transgenic animals uncovered several potential mechanisms. MT suppressed the lysosome formation as well as its function by downregulation of the lysosome-associated genes Lysosome-associated membrane protein 2 (LAMP2), Insulin-like growth factor 2 receptor (IGF2R), and Arylsulfatase B (ARSB). A high level of MT enhanced the antioxidant capacity of these cells to reduce the cell apoptosis induced by the LPS. In addition, the results also uncovered previously unknown information that showed that MT may have protective effects on some human diseases, including tuberculosis, bladder cancer, and rheumatoid arthritis, by downregulation of these disease-associated genes. All these observations warranted further investigations.

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Loss of intraventricular fluid melatonin can explain the neuropathology of Alzheimer's disease

Cited by 28 publications

References 38 publications

Melatonin and mitochondrial function

Melatonin and mitochondrial function

Bright light therapy and melatonin in motor restless behaviour in dementia: a placebo-controlled study

Responses of Transgenic Melatonin-Enriched Goats on LPS Stimulation and the Proteogenomic Profiles of Their PBMCs

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