Alzheimer’s disease research: How Dr. Solomon Carter Fuller contributed | CNN
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Alzheimer’s disease is increasingly widespread, affecting more than 55 million people worldwide — a figure that’s expected to nearly triple by 2050.

Despite the disease’s prevalence, few know the history of research on Alzheimer’s and the role played by an important yet long-overlooked figure: Dr. Solomon Carter Fuller, the first Black psychiatrist and neurologist in the United States.

Fuller’s work “not only advanced the understanding of Alzheimer’s disease, but also exemplified how diverse backgrounds and perspectives in medical research can drive scientific progress and improve patient care across different communities,” said Dr. Chantale Branson, associate professor of neurology at the Morehouse School of Medicine in Atlanta.

  • Paragone@lemmy.worldEnglish
    0·
    1 year ago

    https://pubmed.ncbi.nlm.nih.gov/?term=alzheimer's+virus

    I’m not the poster you’re contempting, I’m just some asshole Empiricist who works to consistently check before contempting.

    Scientific-integrity is not in the culture I grew-up in ( dad’s medical-culture Scientism has no tolerance for it, neither did mom’s Catholicism ),

    but it is required for outright intellectual-integrity.

    For those who won’t check the link to see the results, here is the abstract from 1 paper:

    Infectious agents and Alzheimer’s disease

    Abstract

    Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Individuals affected by the disease gradually lose their capacity for abstract thinking, understanding, communication and memory. As populations age, declining cognitive abilities will represent an increasing global health concern. While AD was first described over a century ago, its pathogenesis remains to be fully elucidated. It is believed that cognitive decline in AD is caused by a progressive loss of neurons and synapses that lead to reduced neural plasticity. AD is a multifactorial disease affected by genetic and environmental factors. The molecular hallmarks of AD include formation of extracellular β amyloid (Aβ) aggregates, neurofibrillary tangles of hyperphosphorylated tau protein, excessive oxidative damage, an imbalance of biothiols, dysregulated methylation, and a disproportionate inflammatory response. Recent reports have shown that viruses (e.g., Herpes simplex type 1, 2, 6A/B; human cytomegalovirus, Epstein-Barr virus, hepatitis C virus, influenza virus, and severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), bacteria (e.g., Treponema pallidum, Borrelia burgdorferi, Chlamydia pneumoniae, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcmitans, Eikenella corrodens, Treponema denticola, and Helicobacter pylori), as well as eukaryotic unicellular parasites (e.g., Toxoplasma gondii) may factor into cognitive decline within the context of AD. Microorganisms may trigger pathological changes in the brain that resemble and/or induce accumulation of Aβ peptides and promote tau hyperphosphorylation. Further, the mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss. Here we review the influence of infectious agents on the development of AD to inspire new research in dementia based on these pathogens.

    bold-highlighting is by me.