More and more studies suggest that infections may be an important cause of dementia and possibly brain aging more generally. The most convincing evidence exists for herpesviruses, which “hibernate” in the nervous system. Recently, an innovative causal approach in data from the United Kingdom has been used to suggest that shingles (herpes zoster) vaccination prevents or delays dementia. To further investigate this, a clinical trial would be needed, but this is costly and time-consuming.
Parkinson’s disease (PD) is the second most common neurodegenerative disease, characterized by progressive motor deficits such as tremor, muscle stiffness, and slowness of movement, affecting six million people worldwide. Despite ongoing efforts to discover the mechanisms underlying this disease, PD remains an incurable disorder. Major challenges include tremendous heterogeneity in disease progression and severity, as well as a lack of reliable, scalable in vitro models to find new therapeutic targets.
Brain resilience—the ability to withstand adverse outcomes despite significant risk factors—is crucial in late-onset Alzheimer’s disease (AD), where the Apolipoprotein E4 (APOE4) gene is a major risk factor. Carrying APOE4 increases AD risk up to 15-fold compared to the ApoE3 allele. Recent single-cell sequencing advancements reveal altered APOE4 expression in various brain cell types, reshaping our understanding of its impact. Despite most APOE4 carriers developing AD, some exhibit resilience, showing normal cognitive function despite pathology.
Current treatments for neurodegenerative disorders (proteinopathies) offer limited efficacy and typically target specific genetic forms. The goal of this research project is to discover targets shared across proteinopathies and advance the development of early diagnostic/prognostic tools and disease-modifying pan-proteinopathy approaches.
Memories are stored at synapses and circuits, which tragically are pruned and deconstructed in Alzheimer's disease (AD). Genetic mutations including APP generate high levels of soluble oligomeric beta amyloid (oAbeta42), leading to insoluble beta amyloid plaques—hallmarks of late-stage disease. Clinical trials have designed "plaque-busting" drugs assuming that plaques cause disease. However, disappointing outcomes demand new approaches. Inflammation is also an AD risk factor, including complement cascade molecules.
Alzheimer’s disease (AD) is the sixth leading cause of death in the United States and there is a tremendous need for improved therapeutic strategies to treat this prevalent neurodegenerative disease. A devastating symptom of AD is progressive memory loss; this particular disease feature has proven difficult to treat. However, research has begun to unravel novel drivers of AD, including the important role the body’s immune system plays in promoting memory loss.
The causes of neurodegenerative disorders like multiple sclerosis or Alzheimer’s disease are incompletely understood, hindering our ability to gain precise diagnoses and design effective therapeutics. Understanding how the circadian rhythms regulate myelin-forming precursors will impart unique insights into normal and aberrant myelination and will have a positive impact on developing therapeutic strategies to restructure myelin.
With an aging population, neurodegenerative disorders contribute increasingly to our global health burden with no cure or effective treatments. Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two neurodegenerative disorders that are distinct in clinical presentation (ALS impairs movement/breathing, whereas FTD impairs behavior/cognition).
There is one characteristic of all neurodegenerative diseases: the accumulation and aggregation of abnormal proteins in the patient’s brain. These aggregations are thought to induce neuronal cell death and brain degeneration.
With an aging population, neurodegenerative disorders contribute increasingly to our global health burden with no cure or effective treatments. Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two neurodegenerative disorders that are distinct in clinical presentation (ALS impairs movement/breathing, whereas FTD impairs behavior/cognition).