What question did this study set out to answer?

To determine whether lipid rafts serve as an early site for amyloid-beta oligomer accumulation and subsequent interactions with apolipoprotein E and tau in Alzheimer's disease.

April 14, 2004Journal of NeuroscienceOpen Access

Dimeric Amyloid β Protein Rapidly Accumulates in Lipid Rafts followed by Apolipoprotein E and Phosphorylated Tau Accumulation in the Tg2576 Mouse Model of Alzheimer's Disease

View Full Paper

Ask AI

Bookmark

To determine whether lipid rafts serve as an early site for amyloid-beta oligomer accumulation and subsequent interactions with apolipoprotein E and tau in Alzheimer's disease.
Isolated lipid rafts from the brains of Tg2576 transgenic mice across an age spectrum spanning young adulthood to 24–28 months.
Analyzed postmortem brain tissue from human Alzheimer's disease patients to validate findings.
Assessed solubility, dimerization, and concentration changes of amyloid-beta, apolipoprotein E, and phosphorylated tau.
Lipid rafts in young mice contain 27% of brain Abeta42 and 24% of Abeta40 despite making up a small fraction of brain volume.
SDS-soluble Abeta dimers appear in lipid rafts at 6 months—concurrent with the onset of memory deficits and prior to plaque formation—and increase >500-fold by 24–28 months.
Accumulation of dimeric Abeta in lipid rafts is sequentially followed by apolipoprotein E and phosphorylated tau accumulation in both Tg2576 mice and human Alzheimer's disease brains.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Preclinical study demonstrates rapid dimeric amyloid-beta accumulation followed by ApoE and phosphorylated tau in lipid rafts of Alzheimer's mice, suggesting lipid rafts drive neurotoxicity.

Cite This Study

Kawarabayashi et al. (2004) studied this question.

synapsesocial.com/papers/6a96b4cc686ece60bb8983aa https://doi.org/10.1523/jneurosci.5543-03.2004

View Full Paper

Ask AI

Bookmark

Implication

Preclinical study demonstrates rapid dimeric amyloid-beta accumulation followed by ApoE and phosphorylated tau in lipid rafts of Alzheimer's mice, suggesting lipid rafts drive neurotoxicity.

Dimeric Amyloid β Protein Rapidly Accumulates in Lipid Rafts followed by Apolipoprotein E and Phosphorylated Tau Accumulation in the Tg2576 Mouse Model of Alzheimer's Disease

Key Points

Discussion

Implication

Cite This Study

Dimeric Amyloid β Protein Rapidly Accumulates in Lipid Rafts followed by Apolipoprotein E and Phosphorylated Tau Accumulation in the Tg2576 Mouse Model of Alzheimer's Disease

Key Points

Discussion

Implication

Cite This Study

Also Consider

Also Consider