LATE‐NCinAlzheimer'sdisease:Molecularaspects and synergies

Author:

Tomé Sandra O.1ORCID,Gawor Klara1,Thal Dietmar Rudolf12ORCID

Affiliation:

1. Laboratory for Neuropathology, Department of Imaging and Pathology and Leuven Brain Institute KU Leuven Leuven Belgium

2. Department of Pathology University Hospitals of Leuven Leuven Belgium

Abstract

AbstractAlzheimer's disease (AD) is classically characterized by senile plaques and neurofibrillary tangles (NFTs). However, multiple copathologies can be observed in the AD brain and contribute to the development of cognitive decline. Limbic‐predominant age‐related TDP‐43 encephalopathy neuropathological changes (LATE‐NC) accumulates in the majority of AD cases and leads to more severe cognitive decline compared with AD pathology alone. In this review, we focus on the synergistic relationship between LATE‐NC and tau in AD, highlighting the aggravating role of TDP‐43 aggregates on tau pathogenesis and its impact on the clinical picture and therapeutic strategies. Additionally, we discuss to what extent the molecular patterns of LATE‐NC in AD differ from frontotemporal lobar degeneration with TDP‐43 pathology (FTLD‐TDP) neuropathological changes. Thus, we highlight the importance of tau and TDP‐43 synergies for subtyping AD patients, which may respond differently to therapeutic interventions depending on the presence of comorbid LATE‐NC.

Funder

Alzheimer Forschung Initiative

Alzheimer's Association

BrightFocus Foundation

Deutsche Forschungsgemeinschaft

Fonds Wetenschappelijk Onderzoek

Internationale Stichting Alzheimer Onderzoek

Onderzoeksraad, KU Leuven

Publisher

Wiley

Subject

Neurology (clinical),Pathology and Forensic Medicine,General Neuroscience

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