Caenorhabditis elegans as an experimental tool for the study of complex neurological diseases: Parkinson’s disease, Alzheimer’s disease and autism spectrum disorder

2011 ◽  
Vol 11 (2) ◽  
pp. 73-83 ◽  
Author(s):  
Fernando Calahorro ◽  
Manuel Ruiz-Rubio
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Autism Spectrum Disorder ◽  
Parkinson's Disease ◽  
Caenorhabditis Elegans ◽  
Neurological Diseases ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Experimental Tool

Caracole as a Potential Neuroprotective Agent for Neurological Diseases: A Systematic

2021 ◽  
Vol 20 ◽  
Author(s):  
Mohammad Zamanian ◽  
Małgorzata Kujawska ◽  
Marjan Nikbakht Zadeh ◽  
Amin Hassanshahi ◽  
Soudeh Ramezanpour ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Neurological Diseases ◽  
Antioxidant Systems ◽  
Neuroprotective Agent ◽  
The Impact

Background & objective: Neurological diseases are becoming a significant problem worldwide, with the elderly at a higher risk of being affected. Several researchers have investigated the neuroprotective effects of Carvacrol (CAR) (5-isopropyl-2-methyl phenol). This review systematically surveys the existing literature on the impact of CAR when used as a neuroprotective agent in neurological diseases. Methods: The systematic review involved English articles published in the last ten years obtained from PubMed, Google Scholar, and Scopus databases. The following descriptors were used to search the literature: “Carvacrol” [Title] AND “neuroprotective (neuroprotection)” [Title] OR “stroke, traumatic brain injury, Alzheimer's disease, Parkinson's disease, seizure, epilepsy [Title]. Results: : A total of 208 articles were retrieved during the search process, but only 20 studies met the eligibility criteria and were included for review. A total of 20 articles were identified, in which the efficacy of CAR was described in experimental models of stroke, traumatic brain injury, Parkinson’s disease, Alzheimer’s disease, , epilepsy, and seizure, through motor deficits improvements in neurochemical activity, especially antioxidant systems, reducing inflammation, oxidative stress and apoptosis as well as inhibition of TRPC1 and TRPM7. Conclusion : The data presented in this study support the beneficial impact of CAR on behavioural and neurochemical deficits. CAR benefits accrue because of its anti-apoptotic, antioxidant, and anti-inflammatory properties. Therefore, CAR has emerged as an alternative treatment for neurological disorders based on its properties.

scholarly journals Aging of the Nigrostriatal Pathway in Humans

1987 ◽  
Vol 14 (S3) ◽  
pp. 424-427 ◽  
Author(s):  
Donald B. Calne ◽  
R.F. Peppard
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurological Diseases ◽  
Nigrostriatal Pathway ◽  
Toxic Damage ◽  
Degenerative Disorders ◽  
The Central Nervous System ◽  
Genetically Determined

ABSTRACT:Progressive degeneration of functionally related groups of neurons occurs in certain infective, toxic, nutritional and genetically determined neurological diseases. It also takes place in normal aging, and several of the regions that undergo selective decay with the passage of time seem to be the same target regions that are afflicted in degenerative disorders such as Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis (ALS). Infective etiology is relatively easy to exclude by a combination of immunological tests and transfer experiments. Genetic causation can be rendered unlikely when large kindreds are available for study. Nutritional deprivation and acute or subacute toxicity are accessible to explanation by examining the environment. The most difficult mechanism of pathogenesis to refute is chronic toxic damage, where the lesion may derive from long-term exposure to a relatively widespread noxious agent or agents. Variations in involvement of individuals within a population may stem from differing capacities to activate or inactivate a toxin. Inherent in this concept of etiology is recognition that compensatory potential within the central nervous system may contribute to prolonged existence of subclinical lesions so that a latent period may exist for several decades, between causal event and the onset of symptoms. Furthermore, progressive clinical deterioration may take place even though the cause may have been transient, many years before. The histological features associated with Parkinson's disease, Alzheimer's disease and ALS may be nonspecific indicators of neuronal “illness”, there being a predilection for certain morphological markers to appear more frequently in particular circumstances and particular regions associated with the pathology of particular diseases.

scholarly journals Disease prediction using graph convolutional networks: Application to Autism Spectrum Disorder and Alzheimer’s disease

2018 ◽  
Vol 48 ◽  
pp. 117-130 ◽  
Author(s):  
Sarah Parisot ◽  
Sofia Ira Ktena ◽  
Enzo Ferrante ◽  
Matthew Lee ◽  
Ricardo Guerrero ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Autism Spectrum Disorder ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Disease Prediction ◽  
Convolutional Networks

Age at death and comorbidity of dementia-related disorders among individuals with autism spectrum disorder

2019 ◽  
Vol 5 (4) ◽  
pp. 293-302 ◽  
Author(s):  
Lucy Barnard-Brak ◽  
David Richman ◽  
Zhanxia Yang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Autism Spectrum Disorder ◽  
General Population ◽  
Vital Statistics ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Age At Death ◽  
Geriatric Population ◽  
Content Type

Purpose Autism spectrum disorder (ASD) is a lifelong disorder that requires intervention and support services for a growing geriatric population. The purpose of this paper is to examine the mean age at death of individuals with ASD and subsequent comorbidity with Alzheimer’s disease, and any form of dementia, as a whole and according to sex. Design/methodology/approach Data consisted of 1,754 individuals who had an ASD listed as one of the causes of deaths from the National Vital Statistics System with data from 1999 to 2015. In the current study, the authors present contradictory results with a mean age at death for individuals with ASD was 68 years by adjusting for changing prevalence rates. Findings Females with ASD had a higher mean age at death than males with ASD; consistent with the trend in the sex differences in the general population. The results of the current study also indicate that individuals with ASD were, in fact, less likely than the general population to have Alzheimer’s disease or a form of dementia. However, males with ASD were significantly more likely to have acquired Alzheimer’s disease or a form of dementia as compared to females with ASD. Originality/value Guan and Li (2017) reported a mean age at death of 36 years old for individuals with ASD, which was subsequently reported in the mass media, most notably CNN. The authors contend that this study provides a more accurate estimate mean age at death.

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