A5000453166- Alzheimer's disease research and treatments
- Intracerebral and Subarachnoid Hemorrhage Research
- Cholinesterase and Neurodegenerative Diseases
- Neurological Disease Mechanisms and Treatments
- Viral-associated cancers and disorders
- Dementia and Cognitive Impairment Research
- Traumatic Brain Injury and Neurovascular Disturbances
- Amyloidosis: Diagnosis, Treatment, Outcomes
- S100 Proteins and Annexins
- Traumatic Brain Injury Research
- Chronic Lymphocytic Leukemia Research
- Cerebrovascular and genetic disorders
- PARP inhibition in cancer therapy
- Enzyme function and inhibition
- Lymphoma Diagnosis and Treatment
- Phosphodiesterase function and regulation
- Mitochondrial Function and Pathology
- Toxin Mechanisms and Immunotoxins
- Cerebrospinal fluid and hydrocephalus
- Tryptophan and brain disorders
- Barrier Structure and Function Studies
- Histiocytic Disorders and Treatments
- Cytomegalovirus and herpesvirus research
- Cell death mechanisms and regulation
- Cutaneous lymphoproliferative disorders research
Temple University
2019-2025
Temple College
2024
New York University
2012-2023
Alzheimer’s Disease Neuroimaging Initiative
2023
Union Bank of Switzerland
2023
NYU Langone Health
2018-2019
University of Florence
2005-2009
Centre International de Recherche sur le Cancer
2006
University of Milan
1988-2002
Ospedale Maggiore
2002
Evidence supporting the hypothesis that reduced cerebrospinal fluid (CSF) clearance is involved in pathophysiology of Alzheimer disease (AD) comes primarily from rodent models. However, unlike rodents, which predominant extracranial CSF egress via olfactory nerves traversing cribriform plate, human pathways are not well characterized. Dynamic PET with <sup>18</sup>F‐THK5117, a tracer for tau pathology, was used to estimate ventricular time–activity as biomarker clearance. We tested 3...
High mobility group proteins are chromatin binding factors with key roles in maintenance of nuclear homeostasis. The evidence indicates that extracellularly released high box 1 (HMGB1) protein behaves as a cytokine, promoting inflammation and participating to the pathogenesis several disorders peripheral organs. In this study, we have investigated expression levels relocation dynamics HMGB1 neural cells, well its neuropathological potential. We report is culture media neurons astrocytes...
Plasma tau may be an accessible biomarker for Alzheimer's disease (AD), but the correlation between plasma and cerebrospinal fluid (CSF) value of combining with CSF phospho-tau (P-tau) are still unclear.Plasma-tau, CSF-tau, P-tau were measured in 97 subjects, including elderly cognitively normal controls (n = 68) patients AD 29) recruited at NYU Center Brain Health, comprehensive neuropsychological magnetic resonance imaging evaluations.Plasma was higher than (P < .001, area under receiver...
A mechanistic understanding of the pathology psychiatric disorders has been hampered by extensive heterogeneity in biology, symptoms, and behavior within diagnostic categories that are defined subjectively. We investigated whether leveraging individual differences information-processing impairments patients with post-traumatic stress disorder (PTSD) could reveal phenotypes disorder. found a subgroup PTSD from two independent cohorts displayed both aberrant functional connectivity ventral...
Cerebrovascular dysfunction has been implicated as a major contributor to Alzheimer's Disease (AD) pathology, with cerebral endothelial cell (cEC) stress promoting ischemia, cerebral-blood flow impairments and blood-brain barrier (BBB) permeability. Recent evidence suggests that cardiovascular (CV)/cerebrovascular risk factors, including hyperhomocysteinemia (Hhcy), exacerbate AD pathology risk. Yet, the underlying molecular mechanisms for this interaction remain unclear. Our lab...
Summary Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer's disease ( AD ). We recently showed carbonic anhydrase inhibitor CAI ) methazolamide MTZ prevents amyloid β (Aβ)‐mediated onset apoptosis mouse brain. In this study, we used and, for first time, analog acetazolamide ATZ neuronal cerebral vascular cells challenged with Aβ, to clarify their protective effects molecular mechanism action. The s selectively inhibited...
Two of the key functions arteries in brain are (1) well-recognized supply blood via vascular lumen and (2) emerging role for arterial walls as routes elimination interstitial fluid (ISF) soluble metabolites, such amyloid beta (Aβ), from retina. As retina possess no conventional lymphatic vessels, drainage toward peripheral lymph nodes is mediated transport along basement membranes capillaries that form intramural peri-arterial (IPAD) system. IPAD tends to fail age but mechanisms underlying...
Impaired clearance in the Alzheimer's Disease (AD) brain is key formation of Aβ parenchymal plaques and cerebrovascular deposits known as cerebral amyloid angiopathy (CAA), present >80% AD patients ~50% non-AD elderly subjects. are highly heterogeneous, containing multiple fragments mostly derived from catabolism Aβ40/Aβ42, which exhibit dissimilar aggregation properties. Remarkably, role these physiologically relevant species injury their impact vascular pathology unknown. We sought to...
Abstract Introduction Cerebrovascular pathology is an early and causal hallmark of Alzheimer's disease (AD), in need effective therapies. Methods Based on the success our previous vitro studies, we tested for first time a model AD cerebral amyloid angiopathy (CAA), carbonic anhydrase inhibitors (CAIs) methazolamide acetazolamide, Food Drug Administration–approved against glaucoma high‐altitude sickness. Results Both CAIs reduced cerebral, vascular, glial beta (Aβ) accumulation caspase...
Cerebral amyloid angiopathy (CAA) is an age-associated condition and a common finding in Alzheimer's disease which amyloid-β (Aβ) vascular deposits are featured >80% of the cases. Familial Aβ variants bearing substitutions at positions 21–23 primarily associated with CAA, although they manifest strikingly different clinical phenotypes: cerebral hemorrhage or dementia. The recently reported Piedmont L34V mutant, located outside hot spot 21–23, shows similar hemorrhagic phenotype, albeit less...
Vascular deposition of amyloid-β (Aβ) in sporadic and familial Alzheimer’s disease, through poorly understood molecular mechanisms, leads to focal ischemia, alterations cerebral blood flow, micro-/macro-hemorrhages, significantly contributing cognitive impairment. Here, we show that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptors DR4 DR5 specifically mediate oligomeric Aβ induction extrinsic apoptotic pathways human microvascular endothelial cells with...
Cerebrospinal fluid (CSF) studies consistently show that CSF levels of amyloid-beta 1–42 (Aβ42) are reduced and tau increased prior to the onset cognitive decline related Alzheimer's disease (AD). However, preclinical prediction accuracy for low Aβ42 levels, a surrogate brain deposits, is not high. Moreover, pathology data suggests course initiated by tauopathy contradicting contemporary clinical view an Aβ cascade. from 3 normal aging cohorts (45–90 years) were combined test both...
Alzheimer’s disease (AD) includes the formation of extracellular deposits comprising aggregated β-amyloid (Aβ) fibers associated with oxidative stress, inflammation, mitochondrial abnormalities, and neuronal loss. There is an associative link between AD cardiac diseases; however, mechanisms underlying potential role AD, particularly Aβ in cells, remain unknown. Here, we investigated mitochondria mediating effects Aβ1-40 Aβ1-42 cultured cardiomyocytes primary coronary endothelial cells. Our...