Publications by authors named "M Iba"
Article Synopsis
- The study investigates the presence of misfolded α-synuclein protein in neurons, a key feature of Parkinson's disease (PD) and dementia with Lewy bodies (DLB), and examines why certain neurons develop this pathology while others do not.
- Using advanced imaging techniques in transgenic mice that overexpress human α-synuclein, researchers identified neuronal cell types in the cortex and hippocampus that are either susceptible or resistant to developing phosphorylated α-synuclein (pSyn) pathology.
- The research also examined gene expression related to α-synuclein processing, revealing specific gene changes linked to mitochondrial and endolysosomal functions that contribute to selective neuronal vulnerability in the context of PD/DLB.
Synucleinopathies are age-related neurological disorders characterized by the abnormal accumulation of α-synuclein (α-syn) in neuronal and non-neuronal cells. It has been proposed that microglial cells play an important role in synucleinopathy neuroinflammation, as well as homeostatically, such as in the clearance of α-syn aggregates in the brain. Here, we examined the effects of microglia on the pathogenesis of synucleinopathies by cell depletion in a mouse model of synucleinopathies.
View Article and Find Full Text PDFArticle Synopsis
- Multiple system atrophy (MSA) is a neurodegenerative disease that leads to symptoms like parkinsonism and ataxia, but its genetic causes are not well understood and treatment options are limited to supportive care.
- A comprehensive study involving the whole genome sequencing of nearly 900 MSA patients and over 7,000 controls discovered four key genetic risk factors associated with the disease.
- The research identified potential susceptibility genes and provided insights into how genetic variations influence gene expression in brain cells, offering a valuable resource for further studies on similar diseases.
The neuroinflammatory process in synucleinopathies of the aging population such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB) involves microglial activation as well as infiltration of the CNS by T cells and natural killer T cells (NKTs). To evaluate the potential of targeting NKT cells to modulate neuroinflammation, we treated α-syn transgenic (tg) mice (e.g.
View Article and Find Full Text PDF