Research Roundup - August 2025
- Penn FTD Center
- Aug 6
- 3 min read
Read the below Research Roundup from Penn FTD Center Postdoctoral Fellow Sheina Emrani, PhD.

Terms to Know:
Neuroinflammation: Inflammation in the brain. Neuroinflammation can be protective in the short term, like in the context of an infection. But when it lasts too long or becomes too intense, it can contribute to worse brain outcomes. The types of brain cells that drive neuroinflammation are called glial cells (astrocytes and microglia).
Cognition: The brain’s ability to think, remember, and focus. It includes skills like memory, attention and concentration, language, and executive functions (higher-order cognitive skills that involve things like planning, multi-tasking problem-solving).
Neurodegenerative diseases: Diseases that gradually damage the brain over time. Common neurodegenerative diseases include Alzheimer’s disease, Lewy Body disease, and frontotemporal lobar degeneration (FTLD), amongst others. These diseases are often caused by buildup of abnormal proteins in the brain. Each disease has its own signature protein. For example, in FTLD, the two most common proteins that cause symptoms are Tau and TAR DNA-binding protein 43 (TDP-43). Over time, these proteins clump together and damage brain cells. After death, these abnormal proteins, called neuropathology, can be seen by examining brain tissue under a microscope.
Clinical syndromes: A collection of signs and symptoms that, when occur together, suggest a particular neurological condition. For example, older adults who first experience significant memory problems are likely to be diagnosed with the clinical syndrome of Alzheimer’s disease. Comparatively, individuals who first show personality changes, like apathy, disinhibition, repetitive behaviors, or trouble with planning and decision making (executive dysfunction), may be diagnosed with behavioral variant frontotemporal dementia (FTD). Often times people with a clinical syndrome of Alzheimer’s disease will have the neurodegenerative disease of Alzheimer’s disease and people with FTD will have FTLD neuropathology.Â
What we knew:
In neurodegenerative diseases like Alzheimer’s disease, chronic neuroinflammation can contribute to worse cognitive outcomes. Neuroinflammation is involved in the progression of FTLD neuropathology. Yet few studies have looked at whether neuroinflammation contributes to worse cognitive outcomes. The few studies (<5) that have looked at the relationship between neuroinflammation and cognition in FTD (the clinical syndrome) suggest that neuroinflammation does worsen cognitive outcomes.
What we didn’t know:
Although previous studies suggest that neuroinflammation may worsen cognitive outcomes in clinical FTD, all lacked confirmation that the underlying neurodegenerative disease was FTLD. As a result, it remains unclear whether neuroinflammation is associated with worse cognitive outcomes specifically in individuals who were diagnosed with FTD during life and had confirmed FTLD neuropathology at autopsy.
What this research/study shows:
In individuals with clinical FTD and confirmed FTLD with Tau neuropathology, we found that neuroinflammation was associated with worse cognitive outcomes—even after accounting for the amount of Tau pathology itself, which is already known to contribute to cognitive decline. This effect was seen both on a global cognitive measure (the Mini-Mental State Examination) and in specific cognitive areas such as language. These findings suggest that neuroinflammation plays an independent role in worsening cognitive outcomes observed during life, beyond the effects of the underlying disease-causing proteins, Tau in this case.
What to do with this information:
These findings suggest that neuroinflammation contributes to worse cognitive outcomes in clinical FTD. Although it remains challenging to determine the exact underlying neurodegenerative disease in individuals with the clinical syndrome of FTD while they are alive, these findings motivate longitudinal studies to measure neuroinflammation in the blood, along with robust cognitive testing, to better understand how and where along the disease trajectory neuroinflammation impacts cognition. Gaining this insight may open the door to therapeutic strategies that target and reduce neuroinflammation—potentially slowing the progression of cognitive decline.