Deze cursusinformatie geeft aan hoe het onderwijs zal verlopen bij pandemieniveau code geel en groen.
Als er tijdens het academiejaar aangepast wordt naar code oranje of rood, zijn er wijzigingen mogelijk o.a. in de gebruikte werk - en evaluatievormen.

Molecular neuropathology

Course Code :2018FBDBIC
Study domain:Biomedical Sciences
Academic year:2020-2021
Semester:1st semester
Contact hours:30
Study load (hours):112
Contract restrictions: Exam contract not possible
Language of instruction:English
Exam period:exam in the 1st semester
Lecturer(s)Samir Kumar-Singh

3. Course contents *

Organization of the Brain, and Cell Structure and Function: This course will re-introduce anatomy and physiology of the human and mouse brain with an emphasis on different brain cell types and their functions

II    Common Neurodegenerative Diseases and Disease-mechanisms: This course will provide a systematic clinicopathological review of the major neurodegenerative diseases of the central nervous system such as Alzheimer’s disease, Frontotemporal dementias, Parkinson’s disease, and Prion disorders. This course will also study and compare human disease with the phenotypes observed in common mouse models simulating these disorders.

III        Molecular Pathology of Aging and Neurodegeneration: This course will address to the neurodegenerative diseases on cellular and molecular level following a “genotype-proteotype-phenotype” approach. In other words, this course will lay emphasis on why a given genetic change should result in an abnormal protein and therefore, a clinical-pathological phenotype. What are gain-of-function or loss-of function mutations and how do they impact on protein? As examples of gain-of-function, Alzheimer’s disease will be compared with other amyloidopathies where extracellular proteins aggregate as amyloid and cause dementia; frontotemporal dementias will be discussed as a tauopathy where abnormal accumulation of tau protein occurs and Parkinson’s disease will be discussed as a synucleinopathy where synuclein protein accumulates abnormally within cells. As an example of loss-of-function mutation, progranulin null-allele mutations that cause frontotemporal dementias will be discussed.