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Evaluating Alzheimer’s Disease
Therapeutics on mitoNEET Expression
Rachel M. Hemmerlin, Kayle J. Marsh, and Dr. Ashley M. Loe

Department of Chemistry, Slippery Rock University of Pennsylvania,
Slippery Rock, PA, United States

Hallmarks of Alzheimer’s Disease (AD)
• Neurodegenerative disease

• Common symptoms include
dementia, cognitive impairment,
and progressive memory loss

• Hallmarks of AD include the
formation of senile plaques and
neurofibrillary tangles

Mitochondrial dysfunction and its role in cells
• Mitochondria play a role in many cell
cycles including energy metabolism,
antioxidant production, and cell
survival
• Mitochondrial dysfunction leads to the
formation of reactive oxygen species
(ROS)

• Impaired mitochondrial pathways
include ATP generation, ROS
formation and defense, calcium
buffering, morphology and dynamics,
mPTP opening, and cytochrome c
release.

Current AD therapeutics
• AD therapeutics are
cholinesterase inhibitors
which inhibit
acetylcholinesterase (AChE)
and therefore increase the
level of available
acetylcholine
• They are limited to alleviating
the symptoms of AD by trying
to counterbalance the
neurotransmitter disturbance

What is mitoNEET and its role in cells
• Outer mitochondrial membrane protein
with iron sulfur clusters
• Plays a role in iron homeostasis,
regulating energy metabolism, formation
of inter-mitochondrial junctions, and
production of ROS
• Novel target for treating mitochondrial
dysfunction and associated diseases

Experiment Scheme

Imaging using Fluorescence Microscopy

Figure 1. N2a cells expressing mitoNEET-GFP (a) exposed to 5 µM (b), 50 µM (c), or 500 µM
(d), donepezil for 24 hours.

Expression of mitoNEET in response to
donepezil, rivastigmine, and galantamine
mitoNEET-GFP ± rivastigmine

200
150
100
50
0
Control

5 µM

50 µM

250
200
150
100
50
0
Control

500 µM

mitoNEET-GFP ± donepezil

0.5 uM

5 uM

50 uM

500 uM

800000
600000
400000
200000

0
500 µM

*

100
50
0
0.1 uM

1 uM

10 uM

100 uM

1200000

1000000
800000
600000
400000
200000

1000000
800000
600000

*

*

400000
200000
0

0
50 µM

*

150

mitoNEET-GFP ± galantamine
Raw Integrated Density

Raw Integrated Density

1000000

5 µM

200

Control

1200000

Control

250

mitoNEET-GFP ± rivastigmine

1200000

Raw Integrated Density

mitoNEET-GFP ± galantamine
Mean Fluorescence Intensity (a.u.)

250

Mean Fluoresence Intensity (a.u.)

Mean Fluorescence Intensity (a.u.)

mitoNEET-GFP ± donepepzil

Control

0.5 uM

5 uM

50 uM

500 uM

Control

0.1 uM

1 uM

10 uM

100 uM

Conclusion and Future Direction
• Donepezil and rivastigmine did not statistically impact the expression whereas
certain concentrations of galantamine slightly statistically down regulated
mitoNEET expression.
• These finding suggest that current AD drugs do not change mitoNEET expression
and therefore do not target or impact mitochondrial dysfunction in cells.
• Future studies will explore the expression of mitoNEET in response to Aβ and
oxidative stress.

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