NEUR40080 Molecular and Cellular Biology of Neurodegenerative Proteinopathies

Academic Year 2019/2020

Proteinopathies are diseases caused by malformed proteins. Many neurodegenerative disorders, including Alzheimer's disease, Huntington's disease, motor neuron disease and Prion disease are proteinopathies that are associated with the aggregation and/or accumulation of one or more malformed proteins. This lecture course will outline recent advances in our understanding of the molecular pathways underpinning these proteinopathies and how results from these studies are driving the development of disease-modifying therapies. Students will be expected to be familiar with recent publications in the field of neurodegenerative proteinopathies for final exam.

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Curricular information is subject to change

Learning Outcomes:

On successful completion of the module students should be able to:
1. Demonstrate a comprehensive understanding of the molecular mechanisms of proteinopathy in neurodegenerative diseases.
2. Discuss in depth the role of protein aggregation and failed protein clearance in neurodegenerative proteinopathies.
3. Critically evaluate recent research findings into the molecula, genetic and cellular disruptions which underpin these disorders.
4. Demonstrate an understanding of the developments in novel therapeutic strategies for neurodegenerative proteinopathies.

Indicative Module Content:

Lectures 1+2 – Huntington protein (NO'S)
Lectures 3+4 – Motor neuron disease (NO'S)
Lecture 5 – Developing therapies for neurodegenerative proteinopathies I (NO'S)
Lecture 6 – Prion Neuroproteinopathies (MS)
Lectures 7+8 – Alzheimer's (MS)
Lectures 9+10 –Parkinson's disease (MS)
Lecture 11 – Prion-like mechanisms in neurodegeration (MS)
Lecture 12 – Developing therapies for neurodegenerative proteinopathies II (NO'S)

Student Effort Hours: 
Student Effort Type Hours


Autonomous Student Learning




Approaches to Teaching and Learning:
In this module we will discuss the most up-do-date developments in our understanding of neurodegenerative disease and how this is feeding into developing novel therapeutic strategies. It will be taught largely by lectures and student reading of suggested literature. There is a tutorial session at which students will be encouraged to discuss how they can best approach expressing the ideas and discoveries that they have learned about into a structured essay. 
Requirements, Exclusions and Recommendations
Learning Recommendations:

A basic understanding of biochemistry and cell biology is recommended.

Module Requisites and Incompatibles
Not applicable to this module.  
Assessment Strategy  
Description Timing Open Book Exam Component Scale Must Pass Component % of Final Grade
Examination: Exit exam 2 hour End of Trimester Exam No Graded No


Carry forward of passed components
Resit In Terminal Exam
Spring Yes - 2 Hour
Please see Student Jargon Buster for more information about remediation types and timing. 
Feedback Strategy/Strategies

• Feedback individually to students, on an activity or draft prior to summative assessment
• Group/class feedback, post-assessment

How will my Feedback be Delivered?

Students are invited to submit a draft answer to a sample question. This is corrected by the lecturer and returned to the student with comments on what they did well and where they can improve. At the end of the module there is a tutorial where the class divides into groups and gives feedback on draft sample answers and ask any questions they may have on how to approach the final exam.

Name Role
Dr Gary Brennan Lecturer / Co-Lecturer
Dr Niamh O'Sullivan Lecturer / Co-Lecturer
Professor Mike Scott Lecturer / Co-Lecturer
Timetabling information is displayed only for guidance purposes, relates to the current Academic Year only and is subject to change.  
Lecture Offering 1 Week(s) - 5, 6, 7, 8, 9 Thurs 12:00 - 12:50
Lecture Offering 1 Week(s) - 5, 6, 7, 8, 9 Tues 11:00 - 11:50
Lecture Offering 1 Week(s) - 5, 6, 7, 8, 9 Wed 10:00 - 10:50