Debomoy Lahiri
Indiana University-Purdue University-Indianapolis, IN·Neuroscience
Alzheimer's disease (AD) is the most common age-related dementia and has no cure, and recent clinical trials have failed. Several proteins tied to the disease rise or fall together as brain cells die.
- Fields
Neuroscience
Genetics
Biochemistry
- Topics
Alzheimer's disease
dementia
neurodegeneration
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Test whether miR153, a small regulatory RNA, silences predicted target sites in messenger RNAs of the REST-153 network (REST, APP, tau, IL1α, IL6), using reporter clones and protein measurements in cultured cells.
- Determine how miR153 changes native protein levels, reactive oxygen species and cell survival, defining its role in the health and growth of neural cells.
- Measure how miR153 treatment alters the REST-153 network, cell vitality and shape in neurons, glia and mixed cultures differentiated from iPSCs of healthy and Alzheimer's donors.
- Assess whether miR153 and its target messenger RNAs and proteins change with disease stage and brain region in AD, MCI and control human brains, modeled against APOE, sex and age.
- Identify SNPs near the MIR153-1 and -2 genes associated with cerebrospinal fluid amyloid-β and phospho-tau levels, using large-scale genomic data, as candidate biomarkers.
More about the research
Could a single molecular switch control many of them at once? This project focuses on microRNAs, short RNA pieces that turn down the production of proteins from specific messenger RNAs. The team has established that one of them, miR153, reduces production of APP (the precursor of amyloid-β), α-synuclein (SNCA) and REST (a protein that silences genes and protects neurons). It does this by binding the untranslated regions of their messenger RNAs.
Why it matters
Alzheimer's disease lacks effective treatments. If miR153 acts as a master controller of several disease proteins, it could become a new therapeutic target for people with Alzheimer's. Genetic variants near the MIR153 genes and levels of network proteins may also serve as biomarkers to predict risk or track disease progression.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Julie Saugstad
Oregon Health & Science University, OR·Neuroscience
Characterize the size and surface marker proteins of cerebrospinal fluid extracellular vesicles from Alzheimer's, Parkinson's and control participants, comparing females vs. males and APOE-e4 vs. APOE-e3 carriers.
Ling Wu
North Carolina Central University, NC·Neuroscience
Validate newly discovered phosphorylated tau (p-tau) markers for early Alzheimer's diagnosis, including distinguishing mild cognitive impairment from normal cognition, in patient plasma and cerebrospinal fluid.
Giuseppina Tesco
Tufts University, MA·Neuroscience
Test whether the ABCA7 p.Ala1527Gly variant lowers ABCA7 protein levels and causes loss of function in iPSC-derived human excitatory neurons, measuring Aβ42/40 ratios, a readout of harmful amyloid-β.
The school
Indiana University-Purdue University-Indianapolis: 25 labs on PI Pages, $89M a year on research, 120 research doctorates a year.
More about Indiana University-Purdue University-Indianapolis
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