Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Data obtained from several studies have shown that mitochondria are involved and play a central role in the progression of several distinct pathological conditions. Morphological alterations and disruptions on the functionality of mitochondria may be related to metabolic and energy deficiency in neurons in a neurodegenerative disorder. Several recent studies demonstrate the linkage between neurodegeneration and mitochondrial dynamics in the spectrum of a promising era called precision mitochondrial medicine. In this review paper, an analysis of the correlation between mitochondria, Alzheimer's disease, and other central nervous system (CNS)-related disorders like the Parkinson's disease and the autism spectrum disorder is under discussion. The role of GTPases like the mfn1, mfn2, opa1, and dlp1 in mitochondrial fission and fusion is also under investigation, influencing mitochondrial population and leading to oxidative stress and neuronal damage.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1007/s12035-018-1397-x | DOI Listing |
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