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.
As a researcher in the field, this article doesn’t really give a good explanation of what’s going on here. Seems to say he just doubted the cause but didn’t provide any other ideas. Researchers right now are thinking the amyloid beta still plays a major part, the issue is free floating amyloid beta, not the plaques. The plaques therefore would just be another symptom of this free floating amyloid beta. Also, it’s surprisingly similar to diabetes, just localized in the brain. So don’t be overweight.
major reason why the cause is in doubt right now is a couple years ago this guy exposed repeated research fraud trying to prove that amyloid plaques were the sole cause of alzheimers which led to over a decade of wasted alzheimers research.
There is a book called “Doctored” that argues that a lot of the foundational research on Alzheimer’s and amyloid plaques was faked. Excerpt:
https://www.sciencefriday.com/articles/doctored-book-excerpt/
Separately, there is supposedly some evidence now that Alzheimer’s is caused by a virus, or by a history of viral infections.
Separately, there is supposedly some evidence now that Alzheimer’s is caused by a virus, or by a history of viral infections.
You got a citation for that?
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.
Scary that asking for a citation is considered contempting by some. That doesn’t back up what the other person said at all though. There’s a huge difference between saying a virus causes AD and saying that infections worsen cognitive decline in AD. I understand not everyone is experienced in reading scientific literature, but it’s important to recognize that and not spread misinformation if you don’t understand what is being described. The closest this paper gets is to connecting two things: infections cause inflammation and inflammation contributes to AD. Both of these things have already been known for a long time. This does not mean AD is a result of a virus or viral infections.
https://duckduckgo.com/?q=alzheimers+virus works for me ;).
