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» Authors » Philip H Stavrides

Philip H Stavrides

Explore the profile of Philip H Stavrides including associated specialties, affiliations and a list of published articles. Areas
Snapshot
Articles 7
Citations 200
Followers 0
Related Specialties
Biology
Neurology
Cell Biology
Top 10 Co-Authors
Ralph A Nixon
Ying Jiang
James Peddy
Sandipkumar Darji
Monika Pawlik
Dun-Sheng Yang
Cynthia Bleiwas
John F Smiley
Ju-Hyun Lee
Anna Pensalfini
Published In
J Neurosci
Autophagy
Cell Rep
Sci Adv
Nat Commun
Affiliations
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Recent Articles
1.
Increased neuronal expression of the early endosomal adaptor APPL1 leads to endosomal and synaptic dysfunction with cholinergic neurodegeneration
Jiang Y, Sachdeva K, Goulbourne C, Berg M, Peddy J, Stavrides P, et al.
bioRxiv . 2024 Sep; PMID: 39345644
Significance Statement: Dysfunction in the endolysosomal system within neurons is a key feature of Alzheimer's disease (AD). Multiple AD risk factors lead to hyperactivity of the early-endosome GTPase rab5, disrupting...
2.
Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by Tyr-phosphorylated APP βCTF
Im E, Jiang Y, Stavrides P, Darji S, Erdjument-Bromage H, Neubert T, et al.
Sci Adv . 2023 Jul; 9(30):eadg1925. PMID: 37494443
Lysosome dysfunction arises early and propels Alzheimer's disease (AD). Herein, we show that amyloid precursor protein (APP), linked to early-onset AD in Down syndrome (DS), acts directly via its β-C-terminal...
3.
Autophagy is a novel pathway for neurofilament protein degradation
Rao M, Darji S, Stavrides P, Goulbourne C, Kumar A, Yang D, et al.
Autophagy . 2022 Sep; 19(4):1277-1292. PMID: 36131358
How macroautophagy/autophagy influences neurofilament (NF) proteins in neurons, a frequent target in neurodegenerative diseases and injury, is not known. NFs in axons have exceptionally long half-lives enabling formation of large...
4.
Preclinical and randomized clinical evaluation of the p38α kinase inhibitor neflamapimod for basal forebrain cholinergic degeneration
Jiang Y, Alam J, Gomperts S, Maruff P, Lemstra A, Germann U, et al.
Nat Commun . 2022 Sep; 13(1):5308. PMID: 36130946
The endosome-associated GTPase Rab5 is a central player in the molecular mechanisms leading to degeneration of basal forebrain cholinergic neurons (BFCN), a long-standing target for drug development. As p38α is...
5.
Endosomal Dysfunction Induced by Directly Overactivating Rab5 Recapitulates Prodromal and Neurodegenerative Features of Alzheimer's Disease
Pensalfini A, Kim S, Subbanna S, Bleiwas C, Goulbourne C, Stavrides P, et al.
Cell Rep . 2020 Nov; 33(8):108420. PMID: 33238112
Neuronal endosomal dysfunction, the earliest known pathobiology specific to Alzheimer's disease (AD), is mediated by the aberrant activation of Rab5 triggered by APP-β secretase cleaved C-terminal fragment (APP-βCTF). To distinguish...
6.
Specific calpain inhibition by calpastatin prevents tauopathy and neurodegeneration and restores normal lifespan in tau P301L mice
Rao M, McBrayer M, Campbell J, Kumar A, Hashim A, Sershen H, et al.
J Neurosci . 2014 Jul; 34(28):9222-34. PMID: 25009256
Tau pathogenicity in Alzheimer's disease and other tauopathies is thought to involve the generation of hyperphosphorylated, truncated, and oligomeric tau species with enhanced neurotoxicity, although the generative mechanisms and the...
7.
Marked calpastatin (CAST) depletion in Alzheimer's disease accelerates cytoskeleton disruption and neurodegeneration: neuroprotection by CAST overexpression
Rao M, Mohan P, Peterhoff C, Yang D, Schmidt S, Stavrides P, et al.
J Neurosci . 2008 Nov; 28(47):12241-54. PMID: 19020018
Increased activity of calpains is implicated in synaptic dysfunction and neurodegeneration in Alzheimer's disease (AD). The molecular mechanisms responsible for increased calpain activity in AD are not known. Here, we...