scholarly journals Control of Neuroinflammation through Radiation-Induced Microglial Changes

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2381
Author(s):  
Alexandra Boyd ◽  
Sarah Byrne ◽  
Ryan J. Middleton ◽  
Richard B. Banati ◽  
Guo-Jun Liu
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Ionising Radiation ◽  
Neuroprotective Effects ◽  
Radiation Induced ◽  
The Central Nervous System ◽  
Inflammatory Molecules ◽  
Microglial Response

Microglia, the innate immune cells of the central nervous system, play a pivotal role in the modulation of neuroinflammation. Neuroinflammation has been implicated in many diseases of the CNS, including Alzheimer’s disease and Parkinson’s disease. It is well documented that microglial activation, initiated by a variety of stressors, can trigger a potentially destructive neuroinflammatory response via the release of pro-inflammatory molecules, and reactive oxygen and nitrogen species. However, the potential anti-inflammatory and neuroprotective effects that microglia are also thought to exhibit have been under-investigated. The application of ionising radiation at different doses and dose schedules may reveal novel methods for the control of microglial response to stressors, potentially highlighting avenues for treatment of neuroinflammation associated CNS disorders, such as Alzheimer’s disease and Parkinson’s disease. There remains a need to characterise the response of microglia to radiation, particularly low dose ionising radiation.

Neurodegenerative diseases and Flavonoids: Special reference to kaempferol

2021 ◽  
Vol 20 ◽  
Author(s):  
Rahul ◽  
Yasir Hasan Siddique
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neuroprotective Effects ◽  
Major Health Problem ◽  
Beneficial Effects

: Neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, Huntington’s disease, Multiple Sclerosis and Ischemic stroke have become a major health problem worldwide. Pre-clinical studies have demonstrated the beneficial effects of flavonoids on neurodegenerative diseases and suggesting them to be used as therapeutic agents. Kaempferol is found in many plants such as tea, beans, broccoli,strawberriesand has neuroprotective effects against the development of many neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease and Huntington's disease. The present study summarizesthe neuroprotective effects of kaempferol in various models of neurodegenerative diseases. Kaempferol delays the initiation as well as the progression of neurodegenerative disorders by acting as a scavenger of free radicals and preserving the activity of various antioxidant enzymes. Kaempferolcan crossthe blood-brain barrier (BBB), and therefore results inan enhanced protective effect. The multi-target property of kaempferol makes it a potential dietary supplement in preventing and treating neurodegenerative diseases.

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 Potential Therapeutic Use of the Rosemary Diterpene Carnosic Acid for Alzheimer’s Disease, Parkinson’s Disease, and Long-COVID through NRF2 Activation to Counteract the NLRP3 Inflammasome

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 124
Author(s):  
Takumi Satoh ◽  
Dorit Trudler ◽  
Chang-Ki Oh ◽  
Stuart A. Lipton
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Nlrp3 Inflammasome ◽  
Carnosic Acid ◽  
Inflammasome Activation ◽  
Neuroprotective Effects ◽  
After Effects ◽  
The Brain

Rosemary (Rosmarinus officinalis [family Lamiaceae]), an herb of economic and gustatory repute, is employed in traditional medicines in many countries. Rosemary contains carnosic acid (CA) and carnosol (CS), abietane-type phenolic diterpenes, which account for most of its biological and pharmacological actions, although claims have also been made for contributions of another constituent, rosmarinic acid. This review focuses on the potential applications of CA and CS for Alzheimer’s disease (AD), Parkinson’s disease (PD), and coronavirus disease 2019 (COVID-19), in part via inhibition of the NLRP3 inflammasome. CA exerts antioxidant, anti-inflammatory, and neuroprotective effects via phase 2 enzyme induction initiated by activation of the KEAP1/NRF2 transcriptional pathway, which in turn attenuates NLRP3 activation. In addition, we propose that CA-related compounds may serve as therapeutics against the brain-related after-effects of SARS-CoV-2 infection, termed “long-COVID.” One factor that contributes to COVID-19 is cytokine storm emanating from macrophages as a result of unregulated inflammation in and around lung epithelial and endovascular cells. Additionally, neurological aftereffects such as anxiety and “brain fog” are becoming a major issue for both the pandemic and post-pandemic period. Many reports hold that unregulated NLRP3 inflammasome activation may potentially contribute to the severity of COVID-19 and its aftermath. It is therefore possible that suppression of NLRP3 inflammasome activity may prove efficacious against both acute lung disease and chronic neurological after-effects. Because CA has been shown to not only act systemically but also to penetrate the blood–brain barrier and reach the brain parenchyma to exert neuroprotective effects, we discuss the evidence that CA or rosemary extracts containing CA may represent an effective countermeasure against both acute and chronic pathological events initiated by SARS-CoV-2 infection as well as other chronic neurodegenerative diseases including AD and PD.

scholarly journals Peroxisome Proliferator-Activated Receptors: A New Ray Of Hope For Parkinson’s Disease

2021 ◽  
Vol 9 (9) ◽  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Peroxisome Proliferator ◽  
Neuroprotective Effects ◽  
In Vivo Models ◽  
Ppar Agonists ◽  
Peroxisome Proliferator Activated Receptors

PD (PD) is a debilitating progressive age-related neurodegenerative disorder that negatively impacts bodily movement. It is the second most common type of neurodegenerative disease after Alzheimer's disease. Although the etiology and pathogenesis of PD remain unknown, a vast body of evidence indicates that oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, and proteasomal dysfunction all play a role in the disease's pathogenesis. Because of the multifactorial nature of the disease, current drug treatment can only offer symptomatic relief and cannot stop or delay the disease progression. The Peroxisome proliferator-activated receptors (PPARs) are the member of the receptor’s superfamily called, nuclear receptors, regulates the growth, differentiation of the tissues, inflammation, mitochondrial function, wound healing, lipid metabolism, and glucose metabolism. Several PPAR agonists have recently been shown to protect neurons from oxidative damage, inflammation, and apoptosis in Alzheimer's disease, PD, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. We review the research on the neuroprotective effects of PPAR agonists in in-vitro and in-vivo models of PD in this paper. Similarly, the pharmacological mechanism of PPAR agonists' neuroprotective effects is examined. Finally, PPAR agonists exert neuroprotective effects by controlling the expression of a set of genes involved in cell survival processes, suggesting that they may be a potential therapeutic target in crippling neurodegenerative diseases like PD. Keywords: Parkinson’s disease, neuroprotective, neuro inflammatory, oxidative stress, PPAR agonist

Neurobehavioral Consequences Associated with Long Term Tramadol Utilization and Pathological Mechanisms

2020 ◽  
Vol 18 (10) ◽  
pp. 758-768 ◽  
Author(s):  
Khadga Raj ◽  
Pooja Chawla ◽  
Shamsher Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Syndrome ◽  
Dopamine Synthesis ◽  
Synthetic Analog

: 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).

scholarly journals Application of deep learning in detecting neurological disorders from magnetic resonance images: a survey on the detection of Alzheimer’s disease, Parkinson’s disease and schizophrenia

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Manan Binth Taj Noor ◽  
Nusrat Zerin Zenia ◽  
M Shamim Kaiser ◽  
Shamim Al Mamun ◽  
Mufti Mahmud
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Deep Learning ◽  
Magnetic Resonance ◽  
Neurological Disorders ◽  
Magnetic Resonance Images ◽  
Future Research ◽  
Comparative Performance

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.

Generalized Rhythmic Delta Activity Frontally Predominant Differentiates Dementia With Lewy Bodies From Alzheimer's Disease and Parkinson's Disease Dementia: A Conventional Electroencephalography Visual Analysis

2021 ◽  
pp. 155005942199714
Author(s):  
Lucia Zinno ◽  
Anna Negrotti ◽  
Chiara Falzoi ◽  
Giovanni Messa ◽  
Matteo Goldoni ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Dementia With Lewy Bodies ◽  
Visual Analysis ◽  
Lewy Bodies ◽  
Delta Activity ◽  
Rhythmic Delta Activity

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.

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