@PrudencioLab

Opinions are my own and not the views of my employer

 Miami, FL
med.miami.edu/faculty/mercedes-prudencio-phd
Joined August 2022
  • Tweets131
  • Following164
  • Followers136
9Media
Advances in HIV treatment have helped people live longer, bringing new questions about how to help them stay healthy as they age. Miller School researchers Drs. Maria Alcaide, Deborah Jones Weiss and Claudia Martinez are studying those questions as part of a long-running national study tracking the health of people living with HIV over time. With the research renewed for another six years, the Miami team is continuing to examine how HIV affects cardiovascular, mental, oral and other aspects of health, with the goal of identifying risks earlier and improving care throughout patients’ lives. Learn more about the research: loom.ly/20jVfFA
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Dr. Mercedes Prudencio and Dr. Leonard Petrucelli have identified an abnormal RNA marker that may help explain why Alzheimer’s disease progresses faster in some people. Higher levels of abnormal UNC13A RNA were linked to greater cognitive impairment and faster decline, offering a potential new way to track disease progression and a target for future therapies. 🧠 Learn more: loom.ly/uFKMNCU
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alz-journals.onlinelibrary.w…

TMEM106B is a selective modulator of TDP‐43 pathology in Alzheimer's disease

INTRODUCTION Co-pathologies – including Lewy body, vascular, and TDP-43 lesions – are common in Alzheimer's disease (AD), contributing to its clinical and pathological heterogeneity. Genetic risk...

alz-journals.onlinelibrary.wiley.com
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Check out our new study! rdcu.be/fzOMO
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alzforum.org/news/research-n…
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Our work on #Microglia and #TDP-43 in early #brain development is finally out @NatureNeuro! Congrats to the brilliant @AnneCompagnion and thanks to the many collaborators!!! Enjoy the read!! :) nature.com/articles/s41593-0…

Microglial TDP-43 mediates myelin refinement and represses Tyrobp cryptic exon inclusion in mice

Nature Neuroscience - Compagnion et al. show that TDP-43 loss in microglia causes myelin defects, oligodendrocyte precursor cell imbalance and motor deficits in mice. They identify TDP-43 as a...

nature.com
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PrudencioLab retweeted
ShorterLab@ShorterLabJun 24
Isoform-specific steric zippers drive aberrant assembly and mislocalization of shortened TDP-43 | Science Advances science.org/doi/10.1126/scia…

Isoform-specific steric zippers drive aberrant assembly and mislocalization of shortened TDP-43

The sequence-encoded determinants underlying aberrant sTDP-43 behavior are defined, revealing therapeutic strategies for ALS.

science.org
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PrudencioLab retweeted
NIH
@NIHJun 10
A team of NIH-funded researchers shed new light on how short RNA molecules prevent abnormal clumping of the TDP-43 protein. These findings, in cell and animal models, suggest RNA-based therapies could one day be used to treat diseases like ALS and Alzheimer’s disease. Learn more: bit.ly/43YLRtc
A neural cell image with blue branching structures on a light blue background. Text overlay reads: "Tiny RNAs show promise for protecting brain cells. NIH-funded research finds short RNA molecules can stop harmful protein clumps, offering a potential new path to treat ALS and related dementias." NIH logo is at the bottom.

ALT A neural cell image with blue branching structures on a light blue background. Text overlay reads: "Tiny RNAs show promise for protecting brain cells. NIH-funded research finds short RNA molecules can stop harmful protein clumps, offering a potential new path to treat ALS and related dementias." NIH logo is at the bottom.

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TDP-43 subtypes shape transcriptomic signatures in Alzheimer's disease biorxiv.org/content/10.64898… @PrudencioLab Excited to share our new transcryptomics study in AD where we use quantiative measures of pathological pTDP-43 and pTau to discern changes resulting from each pathology.

TDP-43 subtypes shape transcriptomic signatures in Alzheimer’s disease

TAR DNA-binding protein 43 (TDP-43) pathology frequently co-occurs with Tau neurofibrillary tangles (NFTs) and amyloid β plaques in Alzheimer’s disease (AD), driving significant clinical heterogene...

biorxiv.org
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Dr. Timothy Miller, 2023 Rainwater Prize winner and Tau Consortium member, leads this @JAMANeuro article reporting long‑term Phase 3 and open‑label extension results in SOD1-ALS. Catch up on this example of bold, patient-focused science: jamanetwork.com/journals/jam…
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PrudencioLab retweeted
ShorterLab@ShorterLabMay 1
Predictive Cellular Signatures from Live Human Motor Neurons Distinguish TDP-43 ALS and Enable ALS Subtype Stratification: biorxiv.org/content/10.64898… – at Philadelphia, PA
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PrudencioLab retweeted
Alzforum@alzforumMay 1
Loss of progranulin drives the buildup of TMEM106B fibrils in lysosomes, causing their membranes to burst. Risk variants in TMEM106B accelerate this process. @UMich @univmiami @NIH @Stanford ow.ly/tW0b50YTw2W
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Dr. Leonard Petrucelli has joined the Miller School of Medicine as Founding Director of the Neuroscience Institute. Dr. Petrucelli is a visionary scientist and a global leader in neurodegeneration research. His seminal work has uncovered the molecular mechanisms underpinning Alzheimer’s disease, frontotemporal dementia and ALS. His research reveals novel biomarkers and therapeutic targets that will help shape the next generation of treatments, helping to improve the lives of patients facing these devastating diseases. Welcome, Dr. Petrucelli! Read more: loom.ly/xQNlf4M
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news.med.miami.edu/leonard-p…

Leonard Petrucelli, Ph.D., Joins Miller School of Medicine as Founding Director of the Neuroscience...

The internationally renowned neuroscientist brings global leadership in Alzheimer’s, ALS and frontotemporal dementia research.

news.med.miami.edu
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The MBI community gathered today to honor longtime colleague Dr. David Borchelt. Dr. Gopal Thinakaran, a close collaborator of Borchelt's, opened the First Annual David R. Borchelt Excellence in Neurodegeneration Research Seminar with a talk on BIN1’s role in Alzheimer’s.
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PrudencioLab retweeted
Target ALS@TargetALS_fdn8 Aug 2025
Tracking #ALS early could transform care. Target ALS-backed scientists are developing blood & CSF tests for #CrypticPeptides—potential early biomarkers. Learn more: bit.ly/45vb0wc #ALSResearch #EveryoneLives
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Dr. Leonard Petrucelli is a globally recognized leader in neurodegeneration and our longtime Scientific Advisor. He's been instrumental in shaping #ALSResearch and the very foundation of Target ALS. As he steps down from his role with us, we celebrate his partnership and vision.
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PrudencioLab retweeted
Gregory Day@GDay_Neuro12 Jun 2025
NEW PAPER is out! We measured plasma p-tau217 and Aβ42/40 in 509 patients with the cognitive concerns. Worth a read if you're thinking of using blood-based biomarkers in the outpatient clinic. doi.org/10.1002/alz.70316 @PiuraYoav1 @MayoClinic @MayoClinicNeuro @mayocliniclabs

Diagnostic performance of plasma p‐tau217 and Aβ42/40 biomarkers in the outpatient memory clinic

INTRODUCTION Plasma biomarkers of Alzheimer's disease (AD) represent accessible alternatives to positron emission tomography (PET) and cerebrospinal fluid (CSF)-based biomarkers in well-characteriz...

alz-journals.onlinelibrary.wiley.com
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mdpi.com/1422-0067/26/11/507…

Evaluating Glial Fibrillary Acidic Protein and Neurofilament Light as Potential Biomarkers for...

Spinocerebellar ataxia type 7 (SCA7), a rare form of ataxia, possesses a wide phenotypic spectrum ranging from classic ataxic symptoms to blindness, multiorgan failure, cardiomyopathy, and early...

mdpi.com
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C9ORF72 poly-PR disrupts expression of ALS/FTD-implicated STMN2 through SRSF7 actaneurocomms.biomedcentral…

C9ORF72 poly-PR disrupts expression of ALS/FTD-implicated STMN2 through SRSF7

Acta Neuropathologica Communications - A hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and...

link.springer.com
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