Ladan Amin, PhD
Instructor
Boston University School of Medicine
Dept of Biochemistry

PhD,
MS, Tabriz University of Medical Sciences




My main research focuses on cellular neuroscience and I am particularly interested in studying the molecular and cellular mechanism underlying neurodegenerative diseases. During my scientific career, I received broad academic training and my research interest shifted from physics to neuroscience. This interdisciplinary background allowed me to develop a good knowledge of the most common biological and biochemical techniques, and enabled me to apply the latest developments in nanotechnology and imaging to neuroscience. My PhD project aimed at unraveling the molecular mechanisms underlying the force generation in neuronal growth cones. To address this issue, I have investigated in detail the role of several important players in force generation such as membrane stiffness, actin turnover and myosin II. As a postdoctoral researcher with Dr. Giuseppe Legname, I was involved in different research projects related to protein misfolding and neurodegenerative diseases. My main research project was focused on defining the physiological function of prion protein (PrP) by analyzing its role on neurite guidance and signaling.

In order to extend my knowledge in neurodegeneration field, I joined Dr. Harris’ Laboratory. I am particularly excited about this opportunity, which complements my previous knowledge by introducing me to the field of Alzheimer’s disease, and is helping me to learn new skills in protein chemistry and cell biology for which the Harris laboratory is known.

Currently, my research project focuses on identifying the molecular mechanism by which amyloid-ß (Aß) aggregates interact with cell surface receptors including cellular prion protein (PrPC). In this work, I am using a multi-disciplinary approach combining single molecule super-resolution microscopy, biochemical and biophysical assays, and cell-based neurotoxicity experiments to measure the dynamics and kinetics of Aß interactions with its membrane receptors. Analyzing several Aß-receptor systems in parallel reveals common molecular mechanisms by which receptors interact with pathologically relevant Aß aggregates to transduce neurotoxic signals. The results of this research are providing new details about Aß aggregation and fibril growth, and they are relevant for developing new therapeutic approaches for Alzheimer’s disease. Moreover, the experimental approaches I use open up the possibility of probing the mechanism of action of other agents that affect Aß aggregation, such as small molecules, inhibitors and antibodies. Altogether, this study is providing important insights into a molecular origin of disease, and the development of therapeutic approaches.


A new approach to visualize the interaction between AB and its receptors
12/01/2018 - 11/30/2022 (PI)
Alzheimer's Association




Title


Yr Title Project-Sub Proj Pubs

Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

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  1. Amin L, Nguyen XT, Rolle IG, D'Este E, Giachin G, Tran TH, Šerbec VC, Cojoc D, Legname G. Characterization of prion protein function by focal neurite stimulation. J Cell Sci. 2016 10 15; 129(20):3878-3891. PMID: 27591261
     
  2. Slapšak U, Salzano G, Amin L, Abskharon RN, Ilc G, Zupancic B, Biljan I, Plavec J, Giachin G, Legname G. The N Terminus of the Prion Protein Mediates Functional Interactions with the Neuronal Cell Adhesion Molecule (NCAM) Fibronectin Domain. J Biol Chem. 2016 Oct 14; 291(42):21857-21868. PMID: 27535221
     
  3. Yousafzai MS, Coceano G, Mariutti A, Ndoye F, Amin L, Niemela J, Bonin S, Scoles G, Cojoc D. Effect of neighboring cells on cell stiffness measured by optical tweezers indentation. J Biomed Opt. 2016 05 31; 21(5):57004. PMID: 27232596
     
  4. Prada I, Amin L, Furlan R, Legname G, Verderio C, Cojoc D. A new approach to follow a single extracellular vesicle-cell interaction using optical tweezers. Biotechniques. 2016 Jan; 60(1):35-41. PMID: 26757810
     
  5. Sayyad WA, Amin L, Fabris P, Ercolini E, Torre V. The role of myosin-II in force generation of DRG filopodia and lamellipodia. Sci Rep. 2015 Jan 19; 5:7842. PMID: 25598228
     
  6. Amin L, Ercolini E, Ban J, Torre V. Comparison of the force exerted by hippocampal and DRG growth cones. PLoS One. 2013; 8(8):e73025. PMID: 23991169
     
  7. Amin L, Ercolini E, Shahapure R, Migliorini E, Torre V. The role of membrane stiffness and actin turnover on the force exerted by DRG lamellipodia. Biophys J. 2012 Jun 06; 102(11):2451-60. PMID: 22713560
     
  8. Amin L, Ercolini E, Sayyad WA, Samadi A, Torre V. The Effect of Blebbistatin and Cytochalasin D on Force Generation in DRG Lamellipodia. Biophysical Journal. 2012; 102(3). View Publication
  9. Amin L, Ercolini E, Shahapure R, Torre V. The Effect of Jasplakinolide and Cyclodextrin on Force Generation in DRG Lamellipodia. Biophysical Journal. 2012; 102(3). View Publication
  10. Amin L, Ercolini E, Shahapure R, Bisson G, Torre V. The elementary events underlying force generation in neuronal lamellipodia. Sci Rep. 2011; 1:153. PMID: 22355669
     
Showing 10 of 14 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 14 publications over 7 distinct years, with a maximum of 4 publications in 2016

YearPublications
20092
20102
20111
20123
20131
20151
20164

Contact for Mentoring:

72 E. Concord Street
Boston MA 02118
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