Nano(Neuro)Medicinal Interventions for Neurodegenerative Disorders: A Meta-Analysis of Concurrent Challenges and

2016 ◽  
pp. 297-336
2019 ◽  
Author(s):  
Giorgia Spaggiari ◽  
Francesco Poti ◽  
Francesca Zimetti ◽  
Ilaria Zanotti ◽  
Daniele Santi

2006 ◽  
Vol 14 (7S_Part_14) ◽  
pp. P768-P768
Author(s):  
Lenka J. Wichmann ◽  
Juan Francisco Flores-Vazquez ◽  
Mengxi Huang ◽  
Ana Luisa Sosa-Ortíz ◽  
André Aleman ◽  
...  

2019 ◽  
Vol 84 ◽  
pp. 238.e25-238.e34 ◽  
Author(s):  
Chrysoula Marogianni ◽  
Dimitrios Rikos ◽  
Antonios Provatas ◽  
Katerina Dadouli ◽  
Panagiotis Ntellas ◽  
...  

Author(s):  
Faraz Ahmad ◽  
Shafiul Haque ◽  
Vishal Chavda ◽  
Ghulam Md Ashraf

: The current meta-analysis of the cohort review was designed to elucidate the progress made in neuroproteomics of the synaptosome. The association of the comprehensive synaptic proteome and its link to physiological or pathological settings is rapidly mounting. Chemical synapses in the brain are focal hot spots for interneuronal signaling, signal transduction, and plasticity. Structurally, synapses comprise axon termini or the presynapse (vesicles filled with neurotransmitters that function as molecular signals), synaptic clefts (extracellular matrix and adhesion molecules), and post-synaptic density or PSD (with receptors for neurotransmitters that rely upon the chemical signaling). The pre- and post-synaptic clefts are responsible for mediating and regulating neurotransmitter release Their receptor binding and perception rely on chemical signals. Moreover, short- and long-term structural and functional alterations that are necessary for the optimal higher-order brain functions are also mainly dependent on the protein dynamics at the synapses. Not surprisingly, disruptions in synaptic physiology are considered as the major pathogenic mechanisms underlying the progression of several neurodegenerative disorders, including Alzheimer's disease. This review briefly discusses the subcellular fractionation protocols and the related biochemical approaches for the isolation of synaptic compartments. Besides, it discusses the progress made in understanding the pathological alterations in the synaptic proteome in neurodegenerative disorders, particularly focussing on Alzheimer's disease dementia.


2020 ◽  
Author(s):  
Henry Yue Hong Meng ◽  
Chi Hang Christopher Mak ◽  
Joyce Wing Yan Mak ◽  
Owen Ho Ko ◽  
Zuo Tao ◽  
...  

2015 ◽  
Vol 27 (9) ◽  
pp. 1429-1438 ◽  
Author(s):  
Zheng-Yu Wang ◽  
Zhen-Min Han ◽  
Qi-Fei Liu ◽  
Wei Tang ◽  
Kui Ye ◽  
...  

ABSTRACTBackground:The etiology and pathogenesis of neurodegenerative disorders has yet to be elucidated, so their differential diagnosis is a challenge. This is especially true in differentiating Alzheimer's disease (AD), dementia with Lewy bodies (DLB), Parkinson disease (PD), and multiple system atrophy (MSA).Methods:A total of 11 eligible articles were identified by search of electronic databases including PubMed, Springer Link, Elsevier, and the Cochrane Library, up to June 2014. In meta-analyses, standardized mean differences (SMD), with 95% confidence intervals (CI), comparing cerebrospinal fluid (CSF) measures of α-synuclein between the above conditions were calculated using random-effects models.Results:CSF α-synuclein concentrations were significantly higher in AD compared to DLB [SMD: 0.32, 95% CI: (0.02, 0.62), z = 2.07, P = 0.038]; PD [SMD: 0.87, 95% CI: (0.15, 1.58), z = 2.38, P = 0.017]; or MSA [SMD: 1.14, 95% CI: (0.15, 2.14), z = 2.25, P = 0.025]. However, no significant difference was found between patients with AD and neurological cognitively normal controls [SMD: 0.02, 95% CI: (−0.21, 0.24), z = 0.13, P = 0.894].Conclusions:Results of these meta-analysis suggest that quantification of CSF α-synuclein could help distinguish AD from other neurodegenerative disorders such as DLB, PD, or MSA.


2021 ◽  
Vol 15 ◽  
Author(s):  
Yoo Jin Jung ◽  
David Tweedie ◽  
Michael T. Scerba ◽  
Dong Seok Kim ◽  
Maria Francesca Palmas ◽  
...  

Neuroinflammation represents a common trait in the pathology and progression of the major psychiatric and neurodegenerative disorders. Neuropsychiatric disorders have emerged as a global crisis, affecting 1 in 4 people, while neurological disorders are the second leading cause of death in the elderly population worldwide (WHO, 2001; GBD 2016 Neurology Collaborators, 2019). However, there remains an immense deficit in availability of effective drug treatments for most neurological disorders. In fact, for disorders such as depression, placebos and behavioral therapies have equal effectiveness as antidepressants. For neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease, drugs that can prevent, slow, or cure the disease have yet to be found. Several non-traditional avenues of drug target identification have emerged with ongoing neurological disease research to meet the need for novel and efficacious treatments. Of these novel avenues is that of neuroinflammation, which has been found to be involved in the progression and pathology of many of the leading neurological disorders. Neuroinflammation is characterized by glial inflammatory factors in certain stages of neurological disorders. Although the meta-analyses have provided evidence of genetic/proteomic upregulation of inflammatory factors in certain stages of neurological disorders. Although the mechanisms underpinning the connections between neuroinflammation and neurological disorders are unclear, and meta-analysis results have shown high sensitivity to factors such as disorder severity and sample type, there is significant evidence of neuroinflammation associations across neurological disorders. In this review, we summarize the role of neuroinflammation in psychiatric disorders such as major depressive disorder, generalized anxiety disorder, post-traumatic stress disorder, and bipolar disorder, as well as in neurodegenerative disorders, such as Parkinson’s disease and Alzheimer’s disease, and introduce current research on the potential of immunomodulatory imide drugs (IMiDs) as a new treatment strategy for these disorders.


2021 ◽  
Vol 12 (2) ◽  
pp. 162
Author(s):  
RathindraNath Bera ◽  
Richik Tripathi ◽  
Bappaditya Bhattacharjee ◽  
AkhileshKumar Singh ◽  
Shweta Kanojia ◽  
...  

2018 ◽  
Vol 13 (6) ◽  
pp. 1815-1834 ◽  
Author(s):  
Simona Raimo ◽  
Gabriella Santangelo ◽  
Alfonsina D’Iorio ◽  
Luigi Trojano ◽  
Dario Grossi

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