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Long-term neurobehavioral and neuroimaging outcomes in athletes with prior concussion(s) and head impact exposure.
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Department of Neurosurgery, Medical College of Wisconsin, Milwaukee, WI, USA.
The long-term health of former athletes with a history of multiple concussions and/or repetitive head impact (RHI) exposure has been of growing interest among the public. The true proportion of dementia cases attributable to neurotrauma and the neurobehavioral profile/sequelae of multiple concussion and RHI exposure among athletes has been difficult to determine. Across three exposure paradigms (i.
View Article and Find Full Text PDFAnti-neuroinflammatory and Neuroprotective Effects of T-006 on Alzheimer's Disease Models by Modulating TLR4-Mediated MyD88/ NF-κB Signaling.
CNS Neurol Disord Drug Targets
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School of Medicine, Foshan University, Foshan, 528000, China.
Introduction: Neuroinflammation derived from the activation of the microglia is considered a vital pathogenic factor of Alzheimer's Disease (AD). T-006, a tetramethylpyrazine derivative, has been found to alleviate cognitive deficits via inhibiting tau expression and phosphorylation in AD transgenic mouse models. Recently, T-006 has been proven to dramatically decrease the levels of total Amyloid β (Aβ) peptide and Glial Fibrillary Acidic Protein (GFAP) and suppress the expression of ionized calcium binding adaptor molecule-1 (Iba-1) in APP/PS1 mice.
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Department of Psychiatry, National Institute of Mental Health and Neuro Sciences, Bangalore, Karnataka, India.
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Department of Pharmaceutics, NIMS Institute of Pharmacy, NIMS University, Jaipur 303121, Rajasthan, India.
Neurodegenerative diseases (NDs) are debilitating disorders characterized by the progressive and selective loss of function or structure in the brain and spinal cord. Both chronic and acute forms of these diseases are associated with significant morbidity and mortality, as they involve the degeneration of neurons in various brain regions. Misfolding and aggregation of amyloid proteins into oligomer and β-sheet rich fibrils share as common hallmark and lead to neurotoxicity.
View Article and Find Full Text PDFTargeting JNK3 for Alzheimer's disease: Design and synthesis of novel inhibitors with aryl group diversity utilizing wide pocket.
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Department of Pharmacy, Institute of Pharmaceutical Science and Technology, College of Pharmacy, Hanyang University, 55 Hanyangdaehak-ro, Sangnok-gu, Ansan, Kyeonggi-do, 15588, Republic of Korea. Electronic address:
JNK3, a brain-specific stress-activated protein kinase, plays a critical role in Alzheimer's disease pathogenesis through phosphorylation of Tau and APP. This study aimed to develop selective JNK3 inhibitors based on a pyrazole scaffold, focusing on (E)-1-(2-aminopyrimidin-4-yl)-4-styryl-1H-pyrazole-3-carboxamide derivatives. Through systematic structural modifications and extensive SAR analysis, we identified compounds 24a and 26a as highly potent JNK3 inhibitors, with IC values of 12 and 19 nM, respectively.
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