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\title{PLOS Science Wednesday: Hi reddit, we're Hui-Chen Lu, Yousuf Ali, Hunter
Allen and we found that people with the NMNAT2 protein had greater
resistance to cognitive decline -- Ask Us Anything!}



\author[1]{PLOSScienceWednesday }%
\author[1]{r/Science AMAs}%
\affil[1]{Affiliation not available}%


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  \date{April 24, 2026}


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\begin{abstract}
Hi Reddit, My name is Hui-Chen Lu and I am a Professor at Indiana
University Bloomington. My research focuses on how neural circuits wire
up during development and how to keep neurons healthy despite various
insults and with aging. The majority of neurons in the brains are born
prenatally and have to stay healthy throughout our lifespan. My name is
Yousuf Ali and I am an assistant scientist in Dr. Lu's lab. My research
focuses on understanding the underlying mechanisms that disrupt cellular
homeostasis and serve as a basis of disease in different
proteinopathies, specifically Alzheimer's disease and tauopathies. My
name is Hunter Allen and I am a research assistant in the lab of Dr.
Hui-Chen Lu at Indiana University Bloomington. I currently head-up
operation of our multi-photon microscope as well manage lab IT functions
and assist with technical and computing activities such as Matlab,
Python, and other programming for data analysis. My name is Hugo Bellen
and I am a Professor at Baylor College of Medicine and a HHMI
Investigator. Our research interests include neuronal
communication/maintenance and development of scientific tools allowing
large scale and efficient scientific discoveries. We recently published
a paper titled ``NMNAT2: HSP90 Complex Mediates Proteostasis in
Proteinopathies'' in PLOS Biology. NMNAT2, or nicotinamide
mononucleotide adenylyl transferase 2, is becoming recognized as a key
neuronal maintenance factor. By examining NMNAT2 levels in brains
donated by more than 500 elderly people whose cognitive function was
tested annually before death, we found higher levels of NMNAT2 in people
who had greater resistance to cognitive decline. People with lower
NMNAT2 were more likely to suffer from dementia, suggesting that the
protein helps preserve neurons related to learning and memory. NMNAT2
exerts both an enzyme function to protect neurons from stress caused by
over-excitation, and a `chaperone' function to combat the misfolded
proteins produced in the brain during aging. Many neurodegenerative
disorders are caused by accumulation of ``misfolded'' proteins that
``clump up'' in the brain in forms often referred to as ``plaques,'' or
``tangles.'' Using mouse and cell culture models, we found that NMNAT2
act as a molecular chaperone and binds to misfolded proteins to prevent
or repair the errors that cause these clumps. Interestingly, its
enzymatic function is required to defend against excitotoxicity. Our
work here suggests that NMNAT2 uses both its chaperone and enzymatic
functions to combat different neuronal insults in a context-dependent
manner. We will be answering your questions at 1pm ET -- Ask Us
Anything!%
\end{abstract}%



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