Zobrazeno 1 - 10
of 35
pro vyhledávání: '"David MacTavish"'
Autor:
Wen Fu, Vlatka Vukojevic, Aarti Patel, Rania Soudy, David MacTavish, David Westaway, Kamaljit Kaur, Valeri Goncharuk, Jack Jhamandas
Publikováno v:
Journal of Neuroinflammation, Vol 14, Iss 1, Pp 1-12 (2017)
Abstract Background Neuroinflammation in the brain consequent to activation of microglia is viewed as an important component of Alzheimer’s disease (AD) pathology. Amyloid beta (Aβ) protein is known to activate microglia and unleash an inflammator
Externí odkaz:
https://doaj.org/article/9a9fa02c523c4fa99cf9b49d41312e22
Publikováno v:
Neurobiology of Disease, Vol 21, Iss 2, Pp 413-420 (2006)
In brains of Alzheimer's disease (AD) patients, expression of the neuropeptide galanin is significantly upregulated and galanin-immunoreactive fibers hypertrophy and hyperinnervate cholinergic neurons of the basal forebrain. However, the role of gala
Externí odkaz:
https://doaj.org/article/47a673c8f781415da9bb5556c8cd704a
Autor:
Wen Fu, Jack H. Jhamandas, Rania Soudy, Rachel A Davey, Jing Yang, Ryoichi Kimura, Jeffrey D Zajac, Aarti Patel, David Westaway, David MacTavish
Publikováno v:
Molecular Neurobiology
Based upon its interactions with amyloid β peptide (Aβ), the amylin receptor, a class B G protein-coupled receptor (GPCR), is a potential modulator of Alzheimer’s disease (AD) pathogenesis. However, past pharmacological approaches have failed to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8c6440906649361b0bae4fb8ede6397c
https://doi.org/10.21203/rs.3.rs-515476/v1
https://doi.org/10.21203/rs.3.rs-515476/v1
Autor:
Aarti Patel, Wen Fu, Jack H. Jhamandas, David MacTavish, Rania Soudy, Rachel A Davey, David Westaway, Kamaljit Kaur, Jeffrey D Zajac
Publikováno v:
Alzheimer's & Dementia : Translational Research & Clinical Interventions
Introduction Amylin receptor serves as a portal for the expression of deleterious effects of amyloid β-protein (Aβ), a key pathologic hallmark of Alzheimer's disease. Previously, we showed that AC253, an amylin receptor antagonist, is neuroprotecti
Publikováno v:
Molecular Neurobiology. 54:748-754
Accumulation of amyloid-β peptide (Aβ) is a pathological hallmark of Alzheimer’s disease (AD). We have previously demonstrated that electrophysiological and neurotoxic effects of Aβ and human amylin are expressed via the amylin receptor. Recentl
Autor:
Richard P. Fahlman, Aarti Patel, Wen Fu, Jack H. Jhamandas, Vishnu Vasanthan, David MacTavish
Publikováno v:
Brain Structure and Function. 221:1845-1860
Accumulation of β-amyloid (Aβ) protein within the brain is a neuropathological hallmark of Alzheimer's disease (AD). One strategy to facilitate Aβ clearance from the brain is to promote Aβ catabolism. Matrix metalloproteinase-9 (MMP-9), a member
Autor:
Jack H. Jhamandas, Vlatka Vukojevic, Aarti Patel, David MacTavish, Rania Soudy, Kamaljit Kaur, Wen Fu, David Westaway, Valeri D. Goncharuk
Publikováno v:
Journal of Neuroinflammation
Journal of Neuroinflammation, Vol 14, Iss 1, Pp 1-12 (2017)
Journal of Neuroinflammation, Vol 14, Iss 1, Pp 1-12 (2017)
Background Neuroinflammation in the brain consequent to activation of microglia is viewed as an important component of Alzheimer’s disease (AD) pathology. Amyloid beta (Aβ) protein is known to activate microglia and unleash an inflammatory cascade
Autor:
Klaus Ballanyi, Wen Fu, David MacTavish, Araya Ruangkittisakul, Glen B. Baker, Jack H. Jhamandas
Publikováno v:
Neuroscience. 250:520-535
Neurons and neighboring astrocytic glia are mostly studied in nervous tissues from rodents whereas less is known on their properties and interactions in the human brain. Here, confocal/multiphoton fluorescence imaging for several hours revealed that
Autor:
Jack H. Jhamandas, David MacTavish
Publikováno v:
Apoptosis. 17:37-47
Deposition of amyloid-beta (Aβ) protein, a 39-43 amino acid peptide, in the brain is a major pathological feature of Alzheimer's disease (AD). We have previously provided evidence that in primary cultures of rat basal forebrain and human fetal neuro
Publikováno v:
The Journal of Neuroscience. 27:9262-9269
Amyloid β (Aβ) protein, a 39–43 amino acid peptide deposited in brains of individuals with Alzheimer's disease (AD), has been shown to interact directly with a number of receptor targets including neuronal nicotinic acetylcholine receptors (nAChR