Giovanna Carello‐Collar

ORCID: 0000-0003-4644-0151
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Dementia and Cognitive Impairment Research
  • Neuroscience and Neuropharmacology Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Bioinformatics and Genomic Networks
  • Medical Imaging Techniques and Applications
  • Tryptophan and brain disorders
  • Functional Brain Connectivity Studies
  • Medicinal Plants and Neuroprotection
  • Health, Environment, Cognitive Aging
  • Diet and metabolism studies
  • Neurological Disease Mechanisms and Treatments
  • Amino Acid Enzymes and Metabolism
  • GABA and Rice Research
  • Autism Spectrum Disorder Research
  • Metabolomics and Mass Spectrometry Studies
  • Neurological diseases and metabolism
  • S100 Proteins and Annexins
  • Genetics and Neurodevelopmental Disorders
  • Genetics, Aging, and Longevity in Model Organisms
  • Nicotinic Acetylcholine Receptors Study
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • Machine Learning in Bioinformatics
  • Cognitive Abilities and Testing
  • Prion Diseases and Protein Misfolding

Universidade Federal do Rio Grande do Sul
2020-2025

Abstract Background Blood-based biomarkers (BBMs) have emerged as promising tools to enhance Alzheimer’s disease (AD) diagnosis. Despite two-thirds of dementia cases occurring in the Global South, research on BBMs has predominantly focused populations from North. This geographical disparity hinders our understanding BBM performance diverse populations. To address this, we evaluated diagnostic properties AD a real-world memory clinic Brazil, one largest countries South. We measured blood and...

10.1101/2025.02.23.24319116 preprint EN medRxiv (Cold Spring Harbor Laboratory) 2025-02-24

Abstract Background Amyloid-β imaging through positron emission tomography (PET) has significantly transformed Alzheimer’s disease (AD) research. [ 11 C]PiB been widely used for β-amyloid plaques due to its high affinity and selectivity amyloid deposits. 18 F]AZD4694 is a more recently developed amyloid-PET agent, which structurally resembles PiB less non-specific binding in the white matter than other F-labeled compounds. The purpose of this study compare vitro properties radiotracers...

10.1186/s13550-025-01216-8 article EN cc-by EJNMMI Research 2025-04-01

Autism spectrum disorder (ASD) is a prevalent neurodevelopmental characterized by several alterations, including disorganized brain cytoarchitecture and excitatory/inhibitory (E/I) imbalance. We aimed to analyze aspects associated with the inhibitory components in ASD, using bioinformatics develop notions about embryonic life tissue analysis for postnatal life. analyzed microarray RNAseq datasets of embryos from different ASD models, demonstrating that regions involved neuronal development...

10.3390/ijms23084075 article EN International Journal of Molecular Sciences 2022-04-07

Alzheimer's disease (AD) is a multifactorial pathology, with most cases having sporadic origin. Recently, knock-in (KI) mouse models, such as the novel humanized amyloid-β (hAβ)-KI, have been developed to better resemble human AD.

10.1016/j.isci.2023.108671 article EN cc-by-nc-nd iScience 2023-12-07

<title>Abstract</title> Experimental evidence suggests that activated microglia induce astrocyte reactivity in neurodegenerative disorders, such as Alzheimer’s disease (AD). Here, we investigated the association between microglial activation and amyloid-β (Aβ) with reactive astrogliosis living AD human brain. We studied 101 individuals across spectrum positron emission tomography (PET) for Aβ aggregation ([<sup>18</sup>F]AZD4694) translocator protein (TSPO) ([<sup>11</sup>C]PBR28), along...

10.21203/rs.3.rs-5184011/v1 preprint EN cc-by Research Square (Research Square) 2024-11-04

Abstract Background Mild Behavioral Impairment (MBI) is a construct developed to capture neuropsychiatric symptoms in individuals early stages of neurodegenerative diseases. The assessment MBI with preclinical cognitive manifestations Brazil still quite limited. aim this study evaluate the MBI‐Checklist (MBI‐C) subjective decline (SCD) and mild impairment (MCI) Brazilian Subjective Cognitive Decline (BRASCODE) cohort southern Brazil. Method BRASCODE currently following unimpaired &gt; 60...

10.1002/alz.093065 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Animal models of amyloidosis have been instrumental in Alzheimer’s disease (AD) research since they can resemble pathophysiological features human AD. Nevertheless, each model is generated through different genetic engineering strategies, resulting distinct phenotypes. In this context, whether AD core molecular programs are conserved among mouse remains to be addressed. Herein, we aimed explore similarities and differences the transcriptomic three amyloidosis. Method We...

10.1002/alz.091666 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background The molecular mechanisms associated with Alzheimer’s Disease (AD) have been extensively studied in mouse models ( Mus musculus) . However, experimental research these is costly and time‐consuming. In this context, the nematode Caenorhabditis elegans C. ) an interesting alternative model for studying AD. Nonetheless, whether of AD share transcriptomic similarities remains unclear. Thus, study aims to investigate transcriptomics overlap between elegan s M. musculus models....

10.1002/alz.092954 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Replacement, Reduction, and Refinement (3R) guidelines propose the use of alternative models to study human diseases. These have high homology are less onerous compared rodents, which dominate Alzheimer’s disease (AD) research. However, it is still necessary investigate whether evolutionary components conserved among AD cross‐species. Thus, we aimed determine similar different core molecular programs biological processes in mouse AD. Methods We searched Gene Expression...

10.1002/alz.092626 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Subjective cognitive decline (SCD) is defined by the presence of complaints in cognitively unimpaired (CU) individuals. Despite being part continuum a neurodegenerative disease, cause complaint quite heterogeneous. Sleep disturbances may be associated with and even objective decline. Therefore, our aim to analyse sleep patients SCD evaluated south‐Brazilian (BRASCODE) cohort. Method We included CU individuals aged &gt; 65 years‐old from BRASCODE Exclusion criteria were...

10.1002/alz.093098 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background To evaluate the in vitro binding properties of [ 11 C]PiB and 18 F]NAV4694 head‐to‐head post‐mortem human brain tissue. Method Autoradiography was used to assess uptake control (CN) Alzheimer’s disease (AD) autopsy‐confirmed tissues. The study focuses on analysis prefrontal cortex, inferior parietal posterior cingulate cortex hippocampus sections CN AD cases. values C]PIB were calculated from regions interest (ROIs) drawn manually mentioned sections. In addition, a...

10.1002/alz.093262 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background A rare reelin gene variant (RELN‐COLBOS mutation) delayed dementia onset in almost 30 years an autosomal dominant Alzheimer’s disease (ADAD) carrier. This patient presented with high amyloid‐β (Aβ) plaque load, but low tau accumulation, suggesting that this single‐nucleotide polymorphism (SNP) RELN conferred a resilience not only to cognitive decline also tauopathy ADAD. However, whether SNPs are protective sporadic (AD) is yet be determined. Thus, we sought examine the...

10.1002/alz.092195 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Glial reactivity is a key phenomenon in Alzheimer’s disease (AD) and closely associated with amyloid‐β (Aβ) pathology. Although compelling experimental data suggest that microglial activation modulates reactive astrogliosis, it remains to be elucidated whether influences the association of Aβ pathology astrogliosis living AD human brain. Here, we tested individuals across aging clinical spectrum. Method We studied 101 participants (62 cognitively unimpaired [CU], 26 mild...

10.1002/alz.092550 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Neurodegeneration is a major pathological feature of Alzheimer’s disease (AD). During this process, it known that not only neurons are affected but also glial cells. However, the biological mechanisms driving brain cellular vulnerability and resilience to neurodegeneration in AD remain elusive. Thus, we aimed investigate transcriptomic profile cell types vulnerable resilient regions. Method We searched microarray datasets Gene Expression Omnibus repository for available...

10.1002/alz.091719 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Astrocytes play a main role in brain energy metabolism, primarily through the metabolic cooperation with neurons. The use of [ 18 F]fluorodeoxyglucose(FDG)‐PET has become valuable indicator neurodegeneration Alzheimer's disease (AD), revealing hypometabolic signature, but it is sensitive to changes astrocyte metabolism. It postulated that activation excitatory amino acid transporter 2 (EAAT2) trigger FDG‐PET uptake astrocytes. However, potential relationship between...

10.1002/alz.092899 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract Background Neurodegenerative diseases (NDs), including Alzheimer's disease (AD), Huntington's (HD), Multiple Sclerosis (MS), and Parkinson's (PD) are characterized by the accumulation of misfolded proteins progressive loss neurons. However, whether a neurodegeneration transcriptomic signature exists remains uncertain. Thus, we aimed to explore differentially expressed genes (DEGs) in common AD, HD, MS, PD. We also seek evaluate effect single nucleotide polymorphisms (SNPs) derived...

10.1002/alz.091792 article EN cc-by Alzheimer s & Dementia 2024-12-01
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