High LDL cholesterol linked to early-onset Alzheimer’s

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Elevated levels of LDL cholesterol has been linked to an increased risk of early-onset Alzheimer’s disease, in those with and without a genetic risk factor. This suggests cholesterol could be an independent risk factor for dementia. Additionally, researchers identified a potential new genetic risk factor for early-onset Alzheimer’s, a rare variant of the APOB gene. READ MORE…
Image shows an alzheimer's brain slice.


A new study reports midlife vascular risk factors are associated with elevated levels of amyloid beta in later life. READ MORE…

Women with larger number of “bridging regions” in the brain and Alzheimer

Alzheimer’s disease affects memory. It is rooted in the gut microbiome according to the latest research.  Bad bacteria, molds, fungus, animal feces, high blood glucose, lipids and parasites can affect the brain which cannot fight these invading microbes.
Most women who have Alzheimer’s have also diabetes and depression.  Stress is also a major factor and lack of sunshine. As stress is higher, the less we can sleep.  Those who stayed home and with less education have less ways to use their memory, the first root cause.

Results of recent analysis showed the architecture of tau networks is different in men and women, with women having a larger number of “bridging regions” that connect various communities in the brain. This difference may allow tau to spread more easily between regions, boosting the speed at which it accumulates and putting women at greater risk for developing Alzheimer’s disease. Source: https://neurosciencenews.com/alzheimers-progression-gender-14499/

Unsterilized milk

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Parasites and microbes need triglycerides or cholesterol to thrive

The requirement of cholesterol for internalization of eukaryotic pathogens like protozoa (Leishmaniasis, Malaria and Toxoplasmosis) and the exchange of cholesterol along with other metabolites during reproduction in Schistosomes (helminths) under variable circumstances are poorly understood. In patients infected with some other helminthes, alterations in the lipid profile have been observed. Also, the mechanisms involved in lipid changes especially in membrane proteins related to parasite infections remain uncertain. Present review of literature shows that parasites induce significant changes in lipid parameters, as has been shown in the in vitro study where substitution of serum by lipid/cholesterol in medium and in experimental models (in vivo). Thus changes in lipid profile occur in patients having active infections with most of the parasites. Membrane proteins are probably involved in such reactions. All parasites may be metabolising cholesterol, but the exact relationship with pathogenic mechanism is not clear. So far, studies suggest that there may be some factors or enzymes, which allow the parasite to breakup and consume lipid/cholesterol. Further studies are needed for better understanding of the mechanisms involved in vivo. The present review analysis the various studies till date and the role of cholesterol in pathogenesis of different parasitic infections.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142336/

During infection significant alterations in lipid metabolism and lipoprotein composition occur. Triglyceride and VLDL cholesterol levels increase, while reduced HDL cholesterol (HDL-C) and LDL cholesterol (LDL-C) levels are observed. More importantly, endotoxemia modulates HDL composition and size: phospholipids are reduced as well as apolipoprotein (apo) A-I, while serum amyloid A (SAA) and secretory phospholipase A2 (sPLA2) dramatically increase, and, although the total HDL particle number does not change, a significant decrease in the number of small- and medium-size particles is observed. Low HDL-C levels inversely correlate with the severity of septic disease and associate with an exaggerated systemic inflammatory response. HDL, as well as other plasma lipoproteins, can bind and neutralize Gram-negative bacterial lipopolysaccharide (LPS) and Gram-positive bacterial lipoteichoic acid (LTA), thus favoring the clearance of these products. HDLs are emerging also as a relevant player during parasitic infections, and a specific component of HDL, namely, apoL-1, confers innate immunity against trypanosome by favoring lysosomal swelling which kills the parasite. During virus infections, proteins associated with the modulation of cholesterol bioavailability in the lipid rafts such as ABCA1 and SR-BI have been shown to favor virus entry into the cells. Pharmacological studies support the benefit of recombinant HDL or apoA-I mimetics during bacterial infection, while apoL-1–nanobody complexes were tested for trypanosome infection. Finally, SR-BI antagonism represents a novel and forefront approach interfering with hepatitis C virus entry which is currently tested in clinical studies. From the coming years, we have to expect new and compelling observations further linking HDL to innate immunity and infections.

Table 1

Mechanisms of parasite–microbiota interactions in the vertebrate gut.

Mechanism category Host factors involved Effect direction Mechanism description (Potential) Consequences Examples showing both mechanism and consequence
Physical changes to the gut Intestinal mucus P > M Helminths, and some protozoa, increase mucus production Increases mucolytic bacteria and bacteria capable of using mucins as a carbon source T. suis (Li et al., ); T. muris (Holm et al., ; Houlden et al., ; Ramanan et al., ); Eimeria (Collier et al., )
Reduces bacteria attachment to the gut epithelium T. trichiura (Broadhurst et al., )
Parasites alter mucus composition and structure Alters food availability, attachment sites, gut flow rates, and access to the epithelium for gut microbes T. muris (Hasnain et al., ); N. brasiliensis(Tsubokawa et al., ); E. histolytica (Hicks et al., ); T. gondii (Kim and Khan, ; Trevizan et al., ); Giardia (Kim and Khan, )
M > P Microbiota affects mucus synthesis Impacts expulsion rate of parasites
Epithelial barrier P > M Parasites damage epithelial tight junctions Allows for microbial translocation across the gut epithelium H. polygyrus (Chen et al., ); T. spiralis (McDermott et al., ); S. venezuelensis(Farid et al., ); N. brasiliensis (Hyoh et al., ); T. gondii (Heimesaat et al., ; Hand et al., ; Cohen and Denkers, ); Giardia (Chen et al., ; Halliez, )
M > P Microbiota strengthens and shapes permeability of mucus barrier Alters the degree of mucosal damage and bacterial translocation that occurs after parasite infection
Epithelial cell turnover P > M Helminths increase epithelial cell turnover Selects for microbes capable of replicating at a high rate
M > P Microbiota mediate cell turnover via SCFAs Impacts parasite colonization and expulsion
Innate immunity Toll-like receptors P > M Helminths increase expression of TLRs Increases activation of responses against microbiota H. polygyrus (Ince et al., ; Friberg et al., ); H. diminuta (Kosik-Bogacka et al., )
M > P Microbiota can prime protective immune responses through TLRs Protects against parasite infection through primed innate immune responses T. gondii (Benson et al., )
Antimicrobial peptides P > M Helminths secrete antimicrobial peptides Protects against harmful immune responses elicited by microbial contact
Inflammasomes P > M Parasites alter inflammasome activation Alters pro-inflammatory cytokine secretion and microbial dysbiosis T. musculis (Chudnovskiy et al., )
M > P Microbiota-derived metabolites activate inflammasomes Creates a pro-inflammatory environment that may aid protozoa clearance, but also increased helminth chronicity
Adaptive immunity Th2 cells P > M Helminths increase Th2 responses Alters mucosal barrier function and impairs TH1 responses leading to an inability to control bacterial replication H. polygyrus (Chen et al., )
M > P Gut microbes inhibit or enhance Th2 responses Alters parasite survival T. muris (Dea-Ayuela et al., )
Treg cells P > M Helminths increase Treg responses Downregulates inflammatory responses against microbiota
Promotes Treg-inducing species H. polygyrus (Reynolds et al., )
Helminths secrete TGF-β mimics to induce Foxp3+ Tregs Downregulates inflammatory responses against microbiota H. polygyrus and T. circumcincta (Grainger et al., )
M > P Gut microbes induce Treg responses Impacts parasite persistence and survival H. polygyrus (Reynolds et al., ; Ohnmacht et al., )
Physical attachment n/a M > P Helminth egg hatching require/is enhanced by bacteria attachment Increases helminth colonization T. muris (Hayes et al., ); T. suis (Vejzagić et al., )
Heterophagy n/a M > P Pathogenic bacteria phagocytosed by parasite induces virulence Increases parasite virulence E. histolytica (Galván-Moroyoqui et al., )
Endosymbiosis n/a M > P Enteric bacteria engulfed by parasite, but not ingested Alters host-parasite immune interaction Giardia (El-Shewy and Eid, )
Secretions n/a P > M Helminth body fluids/secretions have antibacterial and bacteriolytic properties Disrupts microbiota
M > P Gut microbes secrete molecules that inhibit invading parasites Decreases parasite infections Cryptosporidium (Deng et al., ; Foster et al., ; Glass et al., ); Giardia(Pérez et al., ); E. tenella(Tierney et al., )
Ingestion n/a P > M Helminths ingest bacteria from their gut environment Restructures microbiota communities T. muris (White et al., )

Source:  https://link.springer.com/chapter/10.1007/978-3-319-09665-0_15

Alzheimer’s gut bacteria, virus and iron dysregulation

Researchers Identify Virus and Two Types of Bacteria as Major Causes of Alzheimer’s

A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.

This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.

Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.

Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.

“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.

Image shows an old lady looking out of a window.

Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said “The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”

The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.


Source: University of Manchester
Image Credit: The image is adapted from the University of Manchester press release.
Original Research: Full open access editorial for “Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152


Microbes and Alzheimer’s Disease

We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.

AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic

“Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152