Background Neurodegenerative and neuropsychiatric diseases are characterised by complex cellular pathology involving coordinated alterations across multiple subcellular components. Advances in high-co...

Background Loss-of-function mutations in the progranulin (PGRN) gene (GRN) are a major cause of Frontotemporal dementia (FTD), also known as frontotemporal lobar degeneration (FTLD). PGRN is a lysosom...

Alzheimer’s disease (AD) has traditionally been viewed as a central nervous system (CNS)-restricted proteinopathy. Although this neurocentric focus has yielded fundamental insights; it may not fully c...

Background Repetitive exposure to mild traumatic brain injury (r-mTBI) increases the risk for chronic traumatic encephalopathy (CTE) and vascular contributions to cognitive impairment and dementia (VC...

Background Repetitive exposure to mild traumatic brain injury (r-mTBI) increases the risk for chronic traumatic encephalopathy (CTE) and vascular contributions to cognitive impairment and dementia (VC...

Alzheimer’s disease is a leading cause of dementia. In addition to progressive cognitive decline, Alzheimer’s patients experience sleep impairments, specifically deficits in the quantity and quality o...

Background Accumulation of intracellular hyperphosphorylated tau protein into aggregates called neurofibrillary tangles is a hallmark of Alzheimer’s disease (AD) and other neurodegenerative diseases. ...

Many neurodegenerative diseases are characterized by pathological protein aggregation in the brain. Alzheimer’s disease displays amyloid-β and tau inclusions in the form of amyloid-β plaques and tau n...

Background Measurement of different tau species using immunoassays has proven effective for detecting early Alzheimer’s disease (AD) pathology. However, assay performance depends on factors such as th...

Background Despite the identification of numerous genetic risk variants for Alzheimer's disease (AD), mechanisms through which these variants act remain unclear. Identifying specific proteins levels a...

Background Parkinson’s disease (PD) is characterized by the progressive accumulation and spatio-temporal spread of α-synuclein (α-syn) oligomers and a progressive loss of dopaminergic neurons. Many st...

Altered PGRN expression or function has been implicated in a broad spectrum of neurodegenerative disorders, including frontotemporal dementia, Alzheimer’s disease, Parkinson’s disease, amyotrophic lat...

Molecular Neurodegeneration Advances -

Mitochondrial dysfunction, redox imbalance, and excessive reactive oxygen species (ROS) generation are key pathological hallmarks of Parkinson’s disease (PD). The origin of these defects and their con...

Background Parkinson’s disease (PD) involves progressive loss of midbrain dopaminergic (mDA) neurons in the substantia nigra. No disease-modifying treatments exist, only symptomatic relief. Our lab re...

Proteomic studies have identified thousands of protein changes in human Alzheimer’s disease brain tissue, offering significant opportunities for therapeutic and biomarker discovery. In this review, we...

Protein aggregation is a hallmark of many neurodegenerative diseases, exemplified by amyloid plaques and neurofibrillary tangles in Alzheimer’s disease (AD) and Lewy bodies in Parkinson’s disease (PD)...

Misfolding and aggregation of α-synuclein underlies several progressive neurodegenerative disorders for which there are no disease-modifying therapies, most notably Parkinson’s disease. α-Synuclein pa...

Background Alzheimer disease (AD) is characterized by deposition of amyloid-β (Aβ). Decreased Aβ clearance in sporadic AD suggests that enhancing clearance is a potential therapeutic strategy. We prev...

Tau pathology plays a critical role in the onset and progression of multiple neurodegenerative diseases. Although synucleinopathies such as Parkinson’s disease (PD) and dementia with Lewy bodies (DLB)...

Ubiquitin and ubiquitin-like proteins (UBLs) have emerged as critical regulators of protein homeostasis and cellular signaling, processes that are increasingly recognized as central to the pathogenesi...

Apolipoprotein E (APOE) is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD) and encodes a major lipid transporter in the central nervous system (CNS). Although apoE has been s...

Background Understanding synapse-specific effects of neuroinflammation can provide mechanistic and therapeutically relevant insights across the spectrum of neurological diseases. Methods We applied ne...

Microglia, the primary immune cell in the brain, have multiple activation phenotypes involved in broad functions within the brain, playing roles in neurotoxicity/neuroprotection, release of inflammato...

Approved and effective therapies for Alzheimer's disease (AD) are extremely limited given the disease prevalence. Most of the currently approved treatments offer symptom management but do not alter pr...

Background We previously reported that germline complement C3 deletion protected cognition and hippocampal synapses in aged APP/PS1dE9 mice despite increased amyloid plaques. To assess whether global ...

Background Complement component 3 (C3) is increasingly recognized for its role in neurodegenerative processes; however, its specific impact on age-related hippocampal dysfunction remains poorly unders...

Background PLCG2 is associated with the risk of Alzheimer’s disease (AD) through a rare missense polymorphism, rs72824905 (P522R) as well as a common variant, rs12446759, within a long non-coding RNA ...

Metabolomics incorporates information from multiple biological systems and is recognized as an emerging tool for identifying novel multiple sclerosis (MS) biomarkers. While prior studies have linked m...