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DHA-PC and PSD-95 decrease after loss of synaptophysin and before neuronal loss in patients with Alzheimer's disease
Dai Yuki1, Yuki Sugiura2, Nobuhiro Zaima3
11] Department of Cell Biology and Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 431-3192, Japan [2] Research and Development Headquarters, Lion Corporation, 7-2-1 Hirai, Edogawa-ku, Tokyo 132-0035, Japan.
Scientific Reports
|November 21, 2014
Summary
Docosahexaenoic acid-phosphatidylcholines (DHA-PCs) are reduced in Alzheimer
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
- Decreased levels of docosahexaenoic acid-containing phosphatidylcholines (DHA-PCs) have been observed in AD brains.
- Specific PC molecular species, like PC(18:0/22:6), are implicated in AD pathogenesis.
Purpose of the Study:
- To investigate the specific molecular species of phosphatidylcholines (PCs) affected in Alzheimer's disease.
- To determine the relationship between PC(18:0/22:6) levels, amyloid-beta (Aβ) deposition, and disease duration in AD.
- To explore the association of PC(18:0/22:6) reduction with synaptic protein levels and neuronal loss in AD.
Main Methods:
- Utilized matrix-assisted laser desorption/ionization imaging mass spectrometry (MALDI-MSI) on postmortem AD brain tissue.
- Quantified specific PC molecular species, focusing on PC(18:0/22:6).
- Correlated PC levels with amyloid-beta (Aβ) deposition, synaptic protein markers (PSD-95, synaptophysin), and neuronal loss.
Main Results:
- PC(18:0/22:6), a DHA-PC species, was selectively depleted in the gray matter of AD patients.
- PC(18:0/22:6) reduction correlated significantly with disease duration in brain regions with high Aβ deposition.
- This depletion was linked to reduced postsynaptic protein PSD-95 but not presynaptic synaptophysin, and did not correlate with Aβ load or neuronal loss.
Conclusions:
- PC(18:0/22:6) reduction is a specific molecular event in Alzheimer's disease gray matter.
- The findings suggest a sequence of pathological events in AD: Aβ deposition, presynaptic disruption, postsynaptic disruption with PC(18:0/22:6) reduction, and finally neuronal loss.
- PC(18:0/22:6) may serve as a potential biomarker for synaptic dysfunction in Alzheimer's disease.
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