In contrast to the idea that tau phosphorylation is toxic, Ittner et al. (2016) recently showed that specific tau phosphorylation is neuroprotective, phenocopying tau ablation (DeVos et al., 2017), thus highlighting the complex tau biology that underlies neurotoxicity and neuroprotection.
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http://dx.doi.org/10.1016/j.neuron.2017.05.001 | DOI Listing |
Neurochem Res
January 2025
Department of Pharmacology, Central University of Punjab, Ghudda, Bhatinda, Punjab, 151401, India.
Antipsychotic medications are used to treat a psychological condition called 'Schizophrenia'. However, its long-term administration causes irregular involuntary motor movements, targeting the orofacial regions. Glycyrrhizic acid (GA) is a naturally occurring triterpene saponin glycoside obtained from the roots of the Glycyrrhiza glabra (liquorice) plant and well known for its antioxidant, antiapoptotic and neuroprotective abilities.
View Article and Find Full Text PDFBackground: The earliest recognized biomarker of AD is deposition of Aβ amyloid that leads to formation of plaques and may, over time, trigger or at least be followed by gliosis/neuroinflammation and neurofibrillary tangles, accompanied by neurodegenerative changes including neuronal and synaptic loss. We have previously reported that semaphorin 4D (SEMA4D), the major ligand of plexin B receptors expressed on astrocytes, is upregulated in diseased neurons during progression of AD and Huntington's disease (HD). Binding of SEMA4D to PLXNB receptors triggers astrocyte reactivity, leading to loss of neuroprotective homeostatic functions, including downregulation of glutamate and glucose transporters (doi:10.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Background: The blood-brain barrier (BBB) is considered the crucial part of neuroprotection from various neurological insults including infection, inflammation, and neurodegeneration including Alzheimer's disease (AD). The cerebral small vessel disease (CSVD) pathologies especially cerebral microbleeds (CMBs) and gadolinium enhancement might reflect the disruption of BBB. The correlation between BBB permeability measured by cerebrospinal fluid (CSF)/plasma albumin quotient (Qalb) and CSVD biomarkers is poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Chula Neuroscience Center, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
Background: The blood-brain barrier (BBB) is considered the crucial part of neuroprotection from various neurological insults including infection, inflammation, and neurodegeneration including Alzheimer's disease (AD). The cerebral small vessel disease (CSVD) pathologies especially cerebral microbleeds (CMBs) and gadolinium enhancement might reflect the disruption of BBB. The correlation between BBB permeability measured by cerebrospinal fluid (CSF)/plasma albumin quotient (Qalb) and CSVD biomarkers is poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Imperial College London, London, United Kingdom.
Background: Microglial reactivity and neuroinflammation are crucial pathological processes in Alzheimer's Disease (AD). Several attempts to develop a treatment by supressing the immune response in AD have been made, yet these yielded very limited results. Recent studies suggest contrasting effects of microglial reactivity, indicating a biphasic response with both beneficial and deleterious effects at distinct stages of AD.
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