ABBAS ABDALLAH

ABBAS ABDALLAH

University of Massachusetts Medical School

H-index: 7

North America-United States

About ABBAS ABDALLAH

ABBAS ABDALLAH, With an exceptional h-index of 7 and a recent h-index of 6 (since 2020), a distinguished researcher at University of Massachusetts Medical School,

His recent articles reflect a diverse array of research interests and contributions to the field:

Methods of treating amyotrophic lateral sclerosis (als)

Artificial microRNA suppresses C9ORF72 variants and decreases toxic dipeptide repeat proteins in vivo

CRISPR/Cas9-mediated excision of ALS/FTD-causing hexanucleotide repeat expansion in C9ORF72 rescues major disease mechanisms in vivo and in vitro

METHOD FOR TREATMENT OF AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD

ABBAS ABDALLAH Information

University

University of Massachusetts Medical School

Position

___

Citations(all)

864

Citations(since 2020)

402

Cited By

620

hIndex(all)

7

hIndex(since 2020)

6

i10Index(all)

7

i10Index(since 2020)

5

Email

University Profile Page

University of Massachusetts Medical School

Top articles of ABBAS ABDALLAH

Methods of treating amyotrophic lateral sclerosis (als)

Published Date

2024/1/2

Aspects of the disclosure relate to recombinant gene editing complexes comprising a recombinant gene editing protein and guide RNA (gRNA) that specifically hybridizes to a region of a C90RF72 gene (eg, a region flanking a G 4 C 2 repeat or within a exonic region of the gene).

Artificial microRNA suppresses C9ORF72 variants and decreases toxic dipeptide repeat proteins in vivo

Authors

Gabriela Toro Cabrera,Katharina E Meijboom,Abbas Abdallah,Helene Tran,Zachariah Foster,Alexandra Weiss,Nicholas Wightman,Rachel Stock,Tania Gendron,Alisha Gruntman,Anthony Giampetruzzi,Leonard Petrucelli,Robert H Brown Jr,Christian Mueller

Journal

Gene Therapy

Published Date

2023/9/26

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that affects motor neurons, causing progressive muscle weakness and respiratory failure. The presence of an expanded hexanucleotide repeat in chromosome 9 open reading frame 72 (C9ORF72) is the most frequent mutation causing familial ALS and frontotemporal dementia (FTD). To determine if suppressing expression of C9ORF72 gene products can reduce toxicity, we designed a set of artificial microRNAs (amiRNA) targeting the human C9ORF72 gene. Here we report that an AAV9-mediated amiRNA significantly suppresses expression of the C9ORF72 mRNA, protein, and toxic dipeptide repeat proteins generated by the expanded repeat in the brain and spinal cord of C9ORF72 transgenic mice.

CRISPR/Cas9-mediated excision of ALS/FTD-causing hexanucleotide repeat expansion in C9ORF72 rescues major disease mechanisms in vivo and in vitro

Authors

Katharina E Meijboom,Abbas Abdallah,Nicholas P Fordham,Hiroko Nagase,Tomás Rodriguez,Carolyn Kraus,Tania F Gendron,Gopinath Krishnan,Rustam Esanov,Nadja S Andrade,Matthew J Rybin,Melina Ramic,Zachary D Stephens,Alireza Edraki,Meghan T Blackwood,Aydan Kahriman,Nils Henninger,Jean-Pierre A Kocher,Michael Benatar,Michael H Brodsky,Leonard Petrucelli,Fen-Biao Gao,Erik J Sontheimer,Robert H Brown,Zane Zeier,Christian Mueller

Journal

Nature communications

Published Date

2022/10/21

A GGGGCC24+ hexanucleotide repeat expansion (HRE) in the C9ORF72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), fatal neurodegenerative diseases with no cure or approved treatments that substantially slow disease progression or extend survival. Mechanistic underpinnings of neuronal death include C9ORF72 haploinsufficiency, sequestration of RNA-binding proteins in the nucleus, and production of dipeptide repeat proteins. Here, we used an adeno-associated viral vector system to deliver CRISPR/Cas9 gene-editing machineries to effectuate the removal of the HRE from the C9ORF72 genomic locus. We demonstrate successful excision of the HRE in primary cortical neurons and brains of three mouse models containing the expansion (500–600 repeats) as well as in patient-derived iPSC motor neurons and brain organoids (450 …

METHOD FOR TREATMENT OF AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Published Date

2021/1/6

C12N15/113—Non-coding nucleic acids modulating the expression of genes, eg antisense oligonucleotides; Antisense DNA or RNA; Triplex-forming oligonucleotides; Catalytic nucleic acids, eg ribozymes; Nucleic acids used in co-suppression or gene silencing

Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD

Authors

Nadja S Andrade,Melina Ramic,Rustam Esanov,Wenjun Liu,Mathew J Rybin,Gabriel Gaidosh,Abbas Abdallah,Samuel Del’Olio,Tyler C Huff,Nancy T Chee,Sadhana Anatha,Tania F Gendron,Claes Wahlestedt,Yanbin Zhang,Michael Benatar,Christian Mueller,Zane Zeier

Journal

Molecular neurodegeneration

Published Date

2020/12

Background The C9ORF72 hexanucleotide repeat expansion is the most common known genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two fatal age-related neurodegenerative diseases. The C9ORF72 expansion encodes five dipeptide repeat proteins (DPRs) that are produced through a non-canonical translation mechanism. Among the DPRs, proline-arginine (PR), glycine-arginine (GR), and glycine-alanine (GA) are the most neurotoxic and increase the frequency of DNA double strand breaks (DSBs). While the accumulation of these genotoxic lesions is increasingly recognized as a feature of disease, the mechanism(s) of DPR-mediated DNA damage are ill-defined and the effect of DPRs on the efficiency of each DNA DSB repair pathways has not been previously evaluated. Methods and results Using DNA …

See List of Professors in ABBAS ABDALLAH University(University of Massachusetts Medical School)

ABBAS ABDALLAH FAQs

What is ABBAS ABDALLAH's h-index at University of Massachusetts Medical School?

The h-index of ABBAS ABDALLAH has been 6 since 2020 and 7 in total.

What are ABBAS ABDALLAH's top articles?

The articles with the titles of

Methods of treating amyotrophic lateral sclerosis (als)

Artificial microRNA suppresses C9ORF72 variants and decreases toxic dipeptide repeat proteins in vivo

CRISPR/Cas9-mediated excision of ALS/FTD-causing hexanucleotide repeat expansion in C9ORF72 rescues major disease mechanisms in vivo and in vitro

METHOD FOR TREATMENT OF AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD

are the top articles of ABBAS ABDALLAH at University of Massachusetts Medical School.

What is ABBAS ABDALLAH's total number of citations?

ABBAS ABDALLAH has 864 citations in total.

    academic-engine

    Useful Links