Neuro-SysMed-seminar 16. september 2026

Forelesar

Dr. Kristoffer Haugarvoll frå demensnoden (ekstern lenke) til Neuro-SysMed.

Emne

"Alzheimer's Disease and Apolipoprotein E (APOE) – good, bad and targetable"

APOE spiller en nøkkelrolle i utviklingen av Alzheimers sykdom og påvirker blant annet amyloidavleiring, betennelsesprosesser og nervecellenes funksjon. Seminaret gir innsikt i ny forskning på hvordan APOE kan bidra til fremtidige behandlinger.

Påmelding

Påmelding gjerast gjennom denne koplinga (ekstern lenke). Fristen er 14. september kl. 11.00 dersom du vil vere med på lunsjen. Heilt fram til seminaret startar dersom ikkje. 

Tid og stad

Stad: Auditoriet i Armauer Hansens Hus

Når: 16. september 2026 kl. 11:30 - 13:00 (lunsj 11:30 - 12:00).

Samandrag (på engelsk, sidan seminaret er på engelsk):

Alzheimer’s disease (AD) is the leading cause of dementia worldwide, with its prevalence rising rapidly as populations age. Apolipoprotein E (APOE) remains the most important and common genetic risk factor, influencing the majority of AD cases. APOE alleles are also associated with other dementias, such as Parkinson’s disease with dementia (PDD). The APOE ε4 allele substantially increases disease risk, whereas ε2 is protective relative to the common ε3 allele. The ε3 allele is also associated with amyloid deposition and other pathogenic mechanisms of AD, although less strongly than the APOE ε4 allele. These alleles encode three apoE protein isoforms that differ by only two amino acids but exert distinct biological effects. Beyond its central role in lipid transport and cholesterol homeostasis, apoE influences multiple pathways involved in neurodegeneration. ApoE is associated with amyloid-β (Aβ) aggregation and deposition. In addition, apoE isoforms differentially modulate neuroinflammation, synaptic function, vascular integrity, and other Aβ-dependent and independent mechanisms. The complexity of apoE biology presents both challenges and opportunities for therapeutic development.