Reduced Phosphoinositide Concentrations in Anterior Temporal Cortex of Alzheimer‐Diseased Brains
Abstract
Samples of brain anterior temporal cortex from 17 patients with Alzheimer's disease and 18 age-matched controls have been analysed for myo-inositol and the three phosphoinositides. There was significantly less phosphatidylinositol in the Alzheimer samples (1.36 mumol/g wet weight) than in the controls (2.28 mumol/g). The concentrations of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate were also lower in Alzheimer cortex, but differences from the control group were not statistically significant. Free myo-inositol concentrations were 5.11 mumol/g (Alzheimer) and 4.44 mumol/g (control) and again the difference was not significant. The lack of phosphoinositides in Alzheimer temporal cortex may impair receptor function.
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Altered PI(4,5)P2 metabolism is linked to Aβ toxicity.
“Altered PI(4,5)P2 metabolism has been linked to Aβ toxicity [93–95].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [93]
PI(4,5)P2 is reduced in the AD brain.
“Familial AD PSEN1 mutations result in disrupted metabolism of PI(4,5)P2 [95] and PI(4,5)P2 has been reported to be reduced in the AD brain [93].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [93]
The C-terminus of SHIP1 contains a NPxY motif that can bind proteins containing ITIM/ITAM, PTB or SH2 domains, and a proline-rich PxxP motif that contains SH3-binding domains.
“The C-terminus of SHIP1 contains a NPxY motif, which can bind to proteins containing immunoreceptor tyrosine inhibitory motifs (ITIM)/immunoreceptor tyrosine activating motifs (ITAM), phosphotyrosine-binding (PTB) or SH2 domains, as well as a proline-rich PxxP motif that contains SH3-binding domains [47, 93–98] (Fig. 2).”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [93]
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- Authors
- Stokes, C. E., & Hawthorne, J. N.
- Affiliations
- University of Nottingham (GB)
- Corresponding author
- Hawthorne, John N.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1987-04
- Volume
- 48
- Issue
- 4
- Pages
- 1018-1021
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2062034622
- Cited by
- 206
- References
- 0
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 3 · 2023: 8 · 2022: 7 · 2021: 8 · 2020: 6 · 2019: 5 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 5 · 2013: 7 · 2012: 7
- FWCI
- 3.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, phosphoinositides, phosphatidylinositol, phosphatidylinositol 4-phosphate, phosphatidylinositol 4,5-bisphosphate, myo-inositol, anterior temporal cortex, brain lipid metabolism, receptor function
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Female, Humans, Inositol, Male, Phosphatidylinositols, Temporal Lobe, Phosphatidylinositol Phosphates, Phosphatidylinositol 4,5-Diphosphate
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