June 2023
Volume 64, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2023
Microtubule Associated Protein Tau (MAPT) in mouse non-transgenic and transgenic tau mutant (P301S) Alzheimer's Disease lenses
Author Affiliations & Notes
  • Juliet A Moncaster
    Boston University, Boston, Massachusetts, United States
  • Douglas Parsons
    Boston University, Boston, Massachusetts, United States
  • Olga Minaeva
    Boston University, Boston, Massachusetts, United States
  • Lee Goldstein
    Boston University, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Juliet Moncaster None; Douglas Parsons None; Olga Minaeva None; Lee Goldstein Cognoptix, Code C (Consultant/Contractor), Cognoptix, Code P (Patent), Cognoptix, Code R (Recipient), Cognoptix, Code S (non-remunerative)
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2023, Vol.64, 1951. doi:
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    • Get Citation

      Juliet A Moncaster, Douglas Parsons, Olga Minaeva, Lee Goldstein; Microtubule Associated Protein Tau (MAPT) in mouse non-transgenic and transgenic tau mutant (P301S) Alzheimer's Disease lenses. Invest. Ophthalmol. Vis. Sci. 2023;64(8):1951.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : We previously discovered that Aβ accumulates in the cortical/supranuclear region of the lens in people with Alzheimer’s Disease (AD) (Goldstein et al., 2003) and Down Syndrome (DS; (Moncaster et al., 2010). We also demonstrated Aβ in the Tg2576 APP Swedish mutation AD mouse model (Moncaster et al., 2022). Another protein that is involved in AD is Microtubule Associated Protein Tau (MAPT). Tau is expressed in the brain and becomes hyperphosphorylated in AD eventually forming neurofibrillary tangles. Tau has previously been reported to be expressed in the mouse lens (Bai et al., 2007; Zhao et al., 2013) but the results vary depending on the mouse model. Here we investigated whether tau protein was expressed in non-transgenic mouse lenses and in a transgenic tau mutant (P301S) mouse model. We also studied whether cataracts may develop in this P301S tau mutant mouse model.

Methods : P301S tau mutant transgenic and non-transgenic mice were bred and maintained at Boston University School of Medicine. Breeder mice were purchased from Jackson Laboratories, Bar Harbor, ME. Male and Female transgenic and non-transgenic mice were sacrificed throughout their lifespan at ages 3-12 months. Mice were perfused with phosphate buffer saline, lenses were isolated and then imaged under two different sources of light using a D70 digital Nikon camera and a custom-adapted Zeiss stereophotomicroscope. Lenses were then snap frozen and analyzed by Western blotting using a panel of tau antibodies.

Results : P301S transgenic and non-transgenic mouse lenses all expressed tau during their lifespan when analyzed by Western blot. P301S transgenic lenses demonstrated an additional higher molecular weight band compared to the non-transgenic mice. No cataract phenotype was observed in transgenic or non-transgenic mouse lenses.

Conclusions : There was no overt difference in lens phenotype between the P301S transgenic and non-transgenic mice. However, the banding pattern observed by Western blot for P301S transgenic mice compared to non-transgenic was different. Our data suggest the P301S tau mutation affects tau processing but does not result in a cataract phenotype. Based on our current and previous results, the data suggests that Aβ may play a more significant role than tau in lens pathology in AD.

This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.

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