PIPages
Labs

Ju Gao

University of Arizona, AZ·Neuroscience

Dementia affects millions of people and has no cure. Frontotemporal lobar degeneration (FTLD) causes up to 10% of dementias that start in middle age.

Fields

Neuroscience

Biochemistry

Biology

Topics

frontotemporal lobar degeneration

frontotemporal dementia

Alzheimer's disease

Grants
1 known grant, through Aug 2027

What they work on

  1. Test whether raising TMEM106B levels, a gene variant linked to dementia risk, impairs mitochondrial shape, membrane potential and respiration and causes damage in cultured cortical neurons.
  2. Examine how TMEM106B binds the Sigma 1 receptor (SigR1), a regulator of contact sites between mitochondria and the endoplasmic reticulum, and whether this interaction drives mitochondrial dysfunction.
  3. Determine how TMEM106B affects the function of mitochondria-associated endoplasmic reticulum membranes (MAMs), which control calcium signaling, lipid handling and mitochondrial dynamics.

More about the research

People with certain variants of a gene called TMEM106B have a higher risk of FTLD and of Alzheimer's disease, but how the gene raises that risk is unclear. One clue is mitochondria, the cell's energy producers, which malfunction in many brain-degenerating diseases.

Why it matters

Explaining how a known dementia risk gene disrupts mitochondria could clarify how frontotemporal lobar degeneration, Alzheimer's disease and age-related cognitive decline develop. The work could point to new drug targets aimed at restoring mitochondrial function in people with these dementias.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

TMEM106B and Mitochondrial Dysfunction in FTLD and Other Dementia

NIH · Sep 2025 – Aug 2027

Closest labs

Jingjing Liang

University of Arizona, AZ·Neuroscience

Test how Aggregatin, a protein encoded by the Alzheimer's-linked gene FAM222A, controls TDP-43 clumping and toxicity in neurons, using Aggregatin knockout models.

Ying Xu

Rutgers University-New Brunswick, NJ·Neuroscience

Test whether removing PDE2A, an enzyme that breaks down the messengers cAMP and cGMP, from the forebrain protects against pathology and memory deficits, by crossing conditional knockout mice with Alzheimer's transgenic mouse models.

Erin Barnhart

Columbia University, NY·Neuroscience

Compare calcium signals in the cytosol and in the endoplasmic reticulum, the neuron's main calcium store, across defined Drosophila motion vision cell types, using simultaneous in vivo imaging in living flies.

The school

University of Arizona: 36 labs on PI Pages, $1.0B a year on research, 487 research doctorates a year.

More about University of Arizona

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