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Home › Research › Topics › leads

leads

11 studies tagged leads, dated 2004-07-01 to 2023-09-10. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Amyloid and tau-PET in early-onset AD: Baseline data from the Longitudinal Early-onset Alzheimer's Disease Study (LEADS) 2023-09-10
  2. Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration 2023-09-01
  3. The Longitudinal Early-onset Alzheimer's Disease Study (LEADS): Framework and methodology 2021-05-21

Studies

11 studies carry this tag.

Date range

2004 to 2023

Top journals

  • The Journal of neuroscience : the official journal of the Society for Neuroscience 3
  • Alzheimer's & dementia : the journal of the Alzheimer's Association 2
  • Antioxidants & redox signaling 1
  • Cell 1
  • FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1

8 journals in all.

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Amyloid and tau-PET in early-onset AD: Baseline data from the Longitudinal Early-onset Alzheimer's Disease Study (LEADS)

    ✓ Peer-reviewed alzhub usefulness score 66 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2023-09-10 Brain scans and imaging

    LEADS data emphasizes the importance of biomarkers to enhance diagnostic accuracy in EOAD.

  2. Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cell 2023-09-01 Genetics

    Persistent DNA double-strand breaks (DSBs) in neurons are an early pathological hallmark of neurodegenerative diseases including Alzheimer's disease (AD), with the potential to disrupt genome integrity.

  3. The Longitudinal Early-onset Alzheimer's Disease Study (LEADS): Framework and methodology

    ✓ Peer-reviewed alzhub usefulness score 62 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-05-21 Brain scans and imaging

    Patients with early-onset Alzheimer's disease (EOAD) are commonly excluded from large-scale observational and therapeutic studies due to their young age, atypical presentation, or absence of pathogenic mutations.

  4. Loss of Trem2 in microglia leads to widespread disruption of cell coexpression networks in mouse brain

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of aging 2018-05-17 TREM2 and immune genetics

    Rare heterozygous coding variants in the triggering receptor expressed in myeloid cells 2 (TREM2) gene, conferring increased risk of developing late-onset Alzheimer's disease, have been identified.

  5. Discovery of a biomarker and lead small molecules to target r(GGGGCC)-associated defects in c9FTD/ALS

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2014-08-14 Tau biomarkers

    A repeat expansion in C9ORF72 causes frontotemporal dementia and amyotrophic lateral sclerosis (c9FTD/ALS).

  6. The Psen1-L166P-knock-in mutation leads to amyloid deposition in human wild-type amyloid precursor protein YAC transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2012-03-29 Biomarkers

    Genetically engineered mice have been generated to model cerebral β-amyloidosis, one of the hallmarks of Alzheimer disease (AD) pathology, based on the overexpression of a mutated cDNA of the amyloid-β precursor protein (AβPP) or by knock-in of the murine Aβpp gene alone or with presenilin1 mutations.

  7. Mitochondrion-derived reactive oxygen species lead to enhanced amyloid beta formation

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Antioxidants & redox signaling 2012-02-28 Risk genes beyond APOE

    Several lines of evidence show that mitochondrion-derived ROS result in enhanced amyloidogenic amyloid precursor protein processing, and that Aβ itself leads to mitochondrial dysfunction and increased ROS levels.

  8. Infant exposure to lead (Pb) and epigenetic modifications in the aging primate brain: implications for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2011-01-01 Genetics

    The beginnings of late onset Alzheimer's disease (LOAD) are still unknown; however, the progressive and latent nature of neurodegeneration suggests that the triggering event occurs earlier in life.

  9. Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the microglia/macrophage phenotype in amyloid precursor protein transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2008-06-01 Risk genes beyond APOE

    Complement factor C3 is the central component of the complement system and a key inflammatory protein activated in Alzheimer's disease (AD).

  10. Alzheimer's disease (AD)-like pathology in aged monkeys after infantile exposure to environmental metal lead (Pb): evidence for a developmental origin and environmental link for AD

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2008-01-01 Risk genes beyond APOE

    The sporadic nature of Alzheimer's disease (AD) argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown.

  11. Absence of C1q leads to less neuropathology in transgenic mouse models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2004-07-01 Risk genes beyond APOE

    C1q, the recognition component of the classical complement activation pathway, is a multifunctional protein known to be expressed in brain of Alzheimer's disease (AD) patients.

All topic tags with their study counts