Neuroprotective and preventative effects of molecular hydrogen

2020 ◽  
Vol 26 ◽  
Author(s):  
Mami Noda ◽  
Jiankang Liu ◽  
Jiangang Long

: One of the beneficial effects of molecular hydrogen (H2 , hydrogen gas) is neuroprotection and prevention of neurological disorders. It is important and useful if taking H2 every day can prevent or ameliorate the progression of neurodegenerative disorders such as Parkinson’s disease or Alzheimer’s disease, both lacking specific therapeutic drugs. There are several mechanisms how H2 protects neuronal damage. Anti-oxidative, anti-inflammatory, and the regulation of endocrine system via stomach-brain connection seem to play an important role. In cellular and tissue level, H2 appears to prevent the production of reactive oxygen species (ROS), not only hydroxy radical(•OH)but also superoxide. In Parkinson’s disease model mice, chronic intake of H2 causes the release of ghrelin from the stomach. In Alzheimer’s disease model mice, sex-different neuroprotection is observed by chronic intake of H2 . In female mice, declines of estrogen and estrogen receptor- (ER) are prevented by H2 , upregulating brain-derived neurotrophic factor (BDNF) and its receptor, tyrosine kinase receptor B (TrkB). The question how drinking H2 upregulates the release of ghrelin or attenuates the decline of estrogen remains to be investigated. The mechanism how H2 modulates endocrine systems and the fundamental question what or where is the target of H2 needs to be elucidated for better understanding of the effects of H2 .

2020 ◽  
Vol 383 ◽  
pp. 112488 ◽  
Author(s):  
Thiago Medeiros da Costa Daniele ◽  
Pedro Felipe Carvalhedo de Bruin ◽  
Robson Salviano de Matos ◽  
Gabriela Sales de Bruin ◽  
Cauby Maia Chaves ◽  
...  

CNS Spectrums ◽  
2007 ◽  
Vol 12 (1) ◽  
pp. 62-68 ◽  
Author(s):  
A. Joyce Young ◽  
Stephanie Johnson ◽  
David C. Steffens ◽  
P. Murali Doraiswamy

ABSTRACTCoenzyme Q10 (CoQ10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals produced during oxidative phosphorylation in the inner mitochondrial membrane. Oxidative stress, resulting in glutathione loss and oxidative DNA and protein damage, has been implicated in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury. Though most have tended to be pilot studies, there are published preliminary clinical trials showing that CoQ10 may offer promise in many brain disorders. For example, a 16-month randomized, placebo-controlled pilot trial in 80 subjects with mild Parkinson's disease found significant benefits for oral CoQ10 1,200 mg/day to slow functional deterioration. However, to date, there are no published clinical trials of CoQ10 in Alzheimer's disease. Available data suggests that oral CoQ10 seems to be relatively safe and tolerated across the range of 300–2,400 mg/day. Randomized controlled trials are warranted to confirm CoQ10's safety and promise as a clinically effective neuroprotectant.


2020 ◽  
Vol 18 (10) ◽  
pp. 758-768 ◽  
Author(s):  
Khadga Raj ◽  
Pooja Chawla ◽  
Shamsher Singh

: Tramadol is a synthetic analog of codeine used to treat pain of moderate to severe intensity and is reported to have neurotoxic potential. At therapeutic dose, tramadol does not cause major side effects in comparison to other opioid analgesics, and is useful for the management of neurological problems like anxiety and depression. Long term utilization of tramadol is associated with various neurological disorders like seizures, serotonin syndrome, Alzheimer’s disease and Parkinson’s disease. Tramadol produces seizures through inhibition of nitric oxide, serotonin reuptake and inhibitory effects on GABA receptors. Extensive tramadol intake alters redox balance through elevating lipid peroxidation and free radical leading to neurotoxicity and produces neurobehavioral deficits. During Alzheimer’s disease progression, low level of intracellular signalling molecules like cGMP, cAMP, PKC and PKA affect both learning and memory. Pharmacologically tramadol produces actions similar to Selective Serotonin Reuptake Inhibitors (SSRIs), increasing the concentration of serotonin, which causes serotonin syndrome. In addition, tramadol also inhibits GABAA receptors in the CNS has been evidenced to interfere with dopamine synthesis and release, responsible for motor symptoms. The reduced level of dopamine may produce bradykinesia and tremors which are chief motor abnormalities in Parkinson’s Disease (PD).


2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Manan Binth Taj Noor ◽  
Nusrat Zerin Zenia ◽  
M Shamim Kaiser ◽  
Shamim Al Mamun ◽  
Mufti Mahmud

Abstract Neuroimaging, in particular magnetic resonance imaging (MRI), has been playing an important role in understanding brain functionalities and its disorders during the last couple of decades. These cutting-edge MRI scans, supported by high-performance computational tools and novel ML techniques, have opened up possibilities to unprecedentedly identify neurological disorders. However, similarities in disease phenotypes make it very difficult to detect such disorders accurately from the acquired neuroimaging data. This article critically examines and compares performances of the existing deep learning (DL)-based methods to detect neurological disorders—focusing on Alzheimer’s disease, Parkinson’s disease and schizophrenia—from MRI data acquired using different modalities including functional and structural MRI. The comparative performance analysis of various DL architectures across different disorders and imaging modalities suggests that the Convolutional Neural Network outperforms other methods in detecting neurological disorders. Towards the end, a number of current research challenges are indicated and some possible future research directions are provided.


2021 ◽  
pp. 155005942199714
Author(s):  
Lucia Zinno ◽  
Anna Negrotti ◽  
Chiara Falzoi ◽  
Giovanni Messa ◽  
Matteo Goldoni ◽  
...  

Introduction. An easily accessible and inexpensive neurophysiological technique such as conventional electroencephalography may provide an accurate and generally applicable biomarker capable of differentiating dementia with Lewy bodies (DLB) from Alzheimer’s disease (AD) and Parkinson’s disease-associated dementia (PDD). Method. We carried out a retrospective visual analysis of resting-state electroencephalography (EEG) recording of 22 patients with a clinical diagnosis of 19 probable and 3 possible DLB, 22 patients with probable AD and 21 with PDD, matched for age, duration, and severity of cognitive impairment. Results. By using the grand total EEG scoring method, the total score and generalized rhythmic delta activity frontally predominant (GRDAfp) alone or, even better, coupled with a slowing of frequency of background activity (FBA) and its reduced reactivity differentiated DLB from AD at an individual level with an high accuracy similar to that obtained with quantitative EEG (qEEG). GRDAfp alone could also differentiate DLB from PDD with a similar level of diagnostic accuracy. AD differed from PDD only for a slowing of FBA. The duration and severity of cognitive impairment did not differ between DLB patients with and without GRDAfp, indicating that this abnormal EEG pattern should not be regarded as a disease progression marker. Conclusions. The findings of this investigation revalorize the role of conventional EEG in the diagnostic workup of degenerative dementias suggesting the potential inclusion of GRDAfp alone or better coupled with the slowing of FBA and its reduced reactivity, in the list of supportive diagnostic biomarkers of DLB.


Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 371
Author(s):  
Patrycja Pawlik ◽  
Katarzyna Błochowiak

Many neurodegenerative diseases present with progressive neuronal degeneration, which can lead to cognitive and motor impairment. Early screening and diagnosis of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are necessary to begin treatment before the onset of clinical symptoms and slow down the progression of the disease. Biomarkers have shown great potential as a diagnostic tool in the early diagnosis of many diseases, including AD and PD. However, screening for these biomarkers usually includes invasive, complex and expensive methods such as cerebrospinal fluid (CSF) sampling through a lumbar puncture. Researchers are continuously seeking to find a simpler and more reliable diagnostic tool that would be less invasive than CSF sampling. Saliva has been studied as a potential biological fluid that could be used in the diagnosis and early screening of neurodegenerative diseases. This review aims to provide an insight into the current literature concerning salivary biomarkers used in the diagnosis of AD and PD. The most commonly studied salivary biomarkers in AD are β-amyloid1-42/1-40 and TAU protein, as well as α-synuclein and protein deglycase (DJ-1) in PD. Studies continue to be conducted on this subject and researchers are attempting to find correlations between specific biomarkers and early clinical symptoms, which could be key in creating new treatments for patients before the onset of symptoms.


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