De plus en plus d'éléments suggèrent que la maladie d'Alzheimer est liée au diabète de type 2, qui a été décrit comme le « diabète de type 3 ».

Le diabète sucré est caractérisé par une hyperglycémie causée par un manque d'insuline ou une résistance à l'insuline. L'insuline est une hormone chargée d'aider le glucose des aliments à pénétrer dans les cellules pour être utilisé comme source d'énergie. Le diabete est donc familièrement associé à la perte de poids et un appétit vorace. Le diabete est associée au développement de complications secondaires. Des études récentes ont révélé un risque accru de développer un dysfonctionnement cognitif ou une démence chez les patients diabétiques. Le diabète sucré est considéré comme un facteur de risque pour de nombreuses maladies neurodégénératives, dont la maladie d'Alzheimer. Des études ont en effet montré le dysfonctionnement de la signalisation de l'insuline dans le cerveau, c'est à dire que les cellules du cerveau sont affamés par manque de glucose.

Ce stress cellulaire entraîne une augmentation de la phosphorylation de la protéine tau (hyperphosphorylation), ce qui est un biomarqueur de la pathologie de la maladie d'Alzheimer. Ce stress cellulaire modifierait l'activité de la glycogène synthase kinase-3β (GSK-3β) et améliorerait la phosphorylation de tau.

Fait intéressant, plusieurs études in vivo avec des médicaments antidiabétiques oraux et un traitement à l'insuline dans le diabète ont amélioré la fonction cognitive et diminué l'hyperphosphorylation de tau.

La glycogène synthase kinase-3 (GSK-3) est une protéine phosphorylant et inactivant la glycogène synthase. Au contraire l'insuline stimule la glycogène synthase.

Les glycations se produisent principalement dans la circulation sanguine pour une petite proportion des sucres simples absorbés : glucose, fructose et galactose. Les produits finaux de glycation avancée (AGE) sont des protéines ou des lipides qui deviennent glyqués à la suite d'une exposition aux sucres. Certains produits de glycation sont impliqués dans de nombreuses maladies chroniques liées à l'âge, notamment les maladies cardiovasculaires (l'endothélium, le fibrinogène et le collagène sont endommagés) et la maladie d'Alzheimer (les protéines amyloïdes sont des sous-produits des réactions évoluant vers les AGE).

Dans cette étude, les auteurs de l'university Minzu en Mongolie intérieure, étudient les effets des produits finaux de glycation avancée sur les neurones comme modèles de la maladie d'Alzheimer. C'est peut-être une influence culturelle qui les a poussé à s'interroger sur l'intérêt de la calycosine dans la maladie d'Alzheimer. En effet un thérapeute de la cour mongole, Hu Sihui, sous le règne de la dynastie mongole Yuan en Chine, est connu pour son livre Yinshan Zhengyao (Principes importants de la nourriture et des boissons), qui est devenu un classique de la médecine chinoise et de la cuisine chinoise. Il a été le premier à découvrir empiriquement et à décrire clairement les maladies de carence.

La calycosine est une isoflavone O-méthylée. Elle peut être isolée de la racine de l'Astragalus membranaceus mongholicus ainsi que du trèfle rouge. L'Astragalus membranaceus, est une plante à fleurs de la famille des Fabacées et fait partie des 50 herbes fondamentales utilisées dans la médecine traditionnelle mongole.

Le trèfle rouge, est une plante à fleurs, elle aussi de la famille Fabaceae.

Les isoflavones sont des dérivés substitués des isoflavones, un type d'isoflavonoïdes naturels, dont beaucoup agissent comme phytoestrogènes chez les mammifères. Les isoflavones sont produites presque exclusivement par les membres de la famille Fabaceae (égumineuses).

Les résultats in-vitro que les scientifiques rapportent ici révélent que la viabilité des cellules PC12 induites par les AGE augmente lorsqu'elles sont traitées avec de la calycosine.

La lignée cellulaire PC12 est souvent utilisée pour obtenir des d'informations sur les maladies du cerveau. Elle a été utilisé dans la recherche sur l'hypoxie et aussi pour trouver quels fragments de protéine prion causent un dysfonctionnement neuronal.

Les scientifiques ont également observé que les capacités d'apprentissage et de mémoire de rats atteints de la maladie d'Alzheimer, liée à la diabète sucré induite par l'AGE, s'amélioraient dans ces conditions.

L'analyse de ces résultats indique donc que la calycosine peut réguler efficacement à la baisse l'activité de GSK-3β, qui inactive la glycogène synthase, ce qui améliore les effets du diabète.

On peut en déduire que la calycosine peut potentiellement présenter d'importantes propriétés thérapeutiques pouvant être exploitées lors du traitement de la maladie d’Alzheimer, notamment quand elle est liée à un diabète sucré.

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Alzheimer's disease (Alzheimer's disease) is progressive brain disease that affects cognition, memory and behavior.

TDP-43 limbic-predominantly age-related encephalopathy (LATE) is a recently defined common neurodegenerative disorder that mimics the clinical symptoms of Alzheimer's disease.

LATE is a very common condition, typically it affects one third of people older than 75 years of age. This is in contrast to Alzheimer's disease pathology, which tends to level off and perhaps decrease in prevalence among persons beyond age 85 years.

TDP-43 is the major disease protein found in frontotemporal dementia and in amyotrophic lateral sclerosis.

At present, the risk factors involved in LATE and those that differentiate it from Alzheimer's disease are largely unknown.

Managing cardiovascular risk factors, maintaining an active lifestyle, and eating a balanced diet are associated with a reduced risk of AD or a lower rate of cognitive decline. Alcohol consumption is widespread and socially encouraged and is rarely associated with neurodegenerative diseases.

However, alcoholism leads to brain atrophy, and long-term alcohol use can damage almost every organ and system in the body.

Authors of a new article used an algorithmic approach to identify important factors that distinguish patients with LATE and/or Alzheimer's disease from controls with significantly imbalanced data.

They analyzed two ROSMAP and NACC datasets and found that lifetime alcohol consumption was one of the most important lifestyle and environmental factors associated with LATE and Alzheimer's disease, and that their associations varied. In particular, the authors identified a specific subpopulation consisting of APOE-e4 carriers.

The authors found that for this subpopulation, light to moderate alcohol consumption was a protective factor against Alzheimer's disease and LATE, but its protective function against Alzheimer's disease appeared to be stronger than LATE.

The codes for authors' algorithms will be (hopefully) available at https://github.com/xinxingwu-uk/PFV.

Studies in arthropods have revealed the existence of mental maps of their position that are very effective in achieving their objective. These maps make it possible to determine their position and the direction to follow. Scientists call these maps "path integration". Three important discoveries showed how these mental maps were implemented in the mammalian brain. * The first, in the early 1970s, is that hippocampal neurons, called place cells, respond to the position of the animal. * The second, in the early 1990s, is that neurons in neighboring regions, called head direction cells, respond in the direction of the animal's head. This makes it possible to manipulate movement information and see how the location and lead direction cells react. * The third finding was that the organization of neurons in the dorsomedial entorhinal cortex, named grid cells, closely resemble a sheet of squared paper organized in a hexagonal fashion and suggests that place cells can use grid cells to calculate distances. Deficits of path integration, ie of these mental maps, manifest themselves at the onset of Alzheimer's disease. Decades before the expected onset of the disease subtle changes in pathway integration are also present in adults at genetic risk for Alzheimer's disease.

Previous studies of path integration have focused on tasks based on visual cues. The vestibular system is a barosensitive sensory organ, located in the inner ear, which contributes to the sensation of movement and balance in most mammals. So the study of these "path integration" maps must absolutely involve the vestibular system. This is realized in a new study published on MedRxiv, by Gillian Coughlan, Michael Hornberger and their colleagues.

One hundred and fifty participants aged 50-75 were recruited to take part in a research study at the University of East Anglia, Norwich, UK.

Saliva kits were sent to participants home and returned to the university the same day the saliva sample was taken to determine APOE genotype status. Sensor data was collected on the iPad-based assessment tool. The final sample size of 53 included 32 ε3ε3 carriers and 21 cross-sectional ε3ε4 carriers, each of whom completed the background cognitive test and vestibular task on the same day, as well as 3 homozygous APOE-ε4ε4 carriers.

The participants were asked to raise their legs (i.e. without touching the ground) and were turned over by the manipulator. Three seconds after the end of the flip, participants had to point the iPad as precisely as possible in the direction of the starting point, while still wearing the headband and earplugs. The iPad recorded vestibular data: acceleration, rotation and direction.

The scientists' results show impaired vestibular function, a deficiency in people at genetic risk for Alzheimer's disease. Vestibular function differentiated ε3ε4 carriers from ε3ε3 carriers, regardless of demographic background. Machine learning algorithms achieved significant performance in classifying genetic groups based on vestibular function, while univariate statistics failed to identify vestibular differences between APOE groups.

Animal and human studies also suggest a strong anatomical and functional interdependence between the vestibular system and the navigational system. Dysregulation of the vestibular system is associated with deficits in pathway integration.

Vestibular signals that influence pathway integration in preclinical Alzheimer's disease can help identify pathological changes before disease onset and thus guide treatment.

Identifying vestibular contributions to the cognitive phenotype of preclinical Alzheimer's disease is important because vestibular dysfunction is often present with treatable hearing loss. Additionally, vestibular balance training improved spatial orientation in monkeys with severe vestibular damage, suggesting that human adults with vestibular dysfunction, might respond to vestibular implant and/or intensive vestibular training.

Moreover, as the vestibular system has extensive connections with brain regions vulnerable to Alzheimer's disease, including the hippocampus, cingulate cortex, and parietal lobe, vestibular stimulation may indeed improve cognitive performance related to integrity of these brain regions, including disorientation and memory loss due to Alzheimer's disease.

Humans and other mammals have two hippocampi, one in each side of the brain. The hippocampus is part of the limbic system, and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation.

In the human, adult neurogenesis has been shown to occur at low levels, and in only three regions of the brain: the lateral ventricles, the amygdala and the hippocampus.

Hippocampal neurogenesis is impaired in Alzheimer’s disease patients, yet, it is unknown whether new neurons play a causative role in memory deficits. Dans un nouvel article Rachana Mishra, Orly Lazarov and colleagues show that immature neurons were actively recruited into the engram following a hippocampus-dependent task. An engram is the association of neuronal physical areas to external stimulus.

To examine whether the augmentation of adult hippocampal neurogenesis rescues learning and memory deficits in FAD, they generated four mouse model of familial Alzheimer disease with inducible neurogenesis. Bax gene deletion is known to enhance the survival of neural progenitor cells and led to increased neurogenesis. Bax belongs to the BCL2 family members which act as anti- or pro-apoptotic regulators, as usual, involved in a wide variety of cellular activities.

Targeted augmentation of neurogenesis in familial Alzheimer’s disease mice restored the number of new neurons in the engram, the dendritic spine density, and the transcription signature of both immature and mature neurons, ultimately leading to the rescue of memory.

Chemogenetic inactivation of immature neurons following enhanced neurogenesis in Alzheimer’s disease, reversed mouse performance, and diminished memory. Notably, Alzheimer’s disease-linked App, ApoE, and Adam were of the top differentially expressed genes in the engram.

Collectively, these observations suggest that defective neurogenesis contributes to memory failure in Alzheimer’s disease.

First is the direct evidence that immature neurons in the DG play a role in hippocampus-dependent memory engram in wild-type and FAD mice.

Second, impairments in hippocampal neurogenesis cause defective engram formation in FAD and underlie memory deficits.

Third, an increasing level of neurogenesis rescues memory by restoring the engram.

Fourth, immature neurons are required for proper memory formation in FAD.

Fifth, augmenting neurogenesis rescues deficits in spine density in both immature and mature engram neurons in the DG of FAD mice.

Sixth, augmenting neurogenesis modulates the profile of immature and mature engram neurons in the DG to resemble the transcription profile of engram cells in wild-type mice.

Seventh, AD-linked signals, particularly App, Apoe, and Adam, play a role in the engram and are modulated following augmentation of neurogenesis and rescue of memory.

Iron accumulates in the brain with age and catalyzes free radical damage to neurons, thus playing a pathogenic role in Alzheimer's disease. To decrease the incidence of Alzheimer's disease, the authors synthesized the iron-affinitive peptide 5YHEDA to scavenge the excess iron in the senile brain: YHEDAYHEDAYHEDAYHEDAYHEDA.

However, the blood-brain barrier (a layer of cells around blood vessels in central nervous system) blocks the entrance of macromolecules into the brain, thus decreasing the therapeutic effects. Several receptors present in the BBB, including transferrin, the insulin receptor, and the low-density lipoprotein receptor (LDLR), are known to allow the passage of cognate protein ligands into the brain

To facilitate the entrance of the 5YHEDA peptide, the authors linked the low-density lipoprotein receptor-binding segment of ApoB-100 to 5YHEDA. Apolipoprotein B-100 (ApoB-100) is a lipid carrier. When recognized and bound by LDLR at the BBB, the complex can be converted to an endosome, subsequently resulting in transcytosis to the abluminal side of the BBB.

There, the apolipoprotein can be released for uptake by neurons and/or astrocytes when the pH is reduced, and the receptor is recycled to the cell surface.

Lipid-interactive regions and LDLR-binding regions are scattered in ApoB-100. The primary LDLR-binding region is located between amino acids 3359 and 3367, which consists of nine amino residues with the sequence “QSDIVAHLL”. To facilitate transport of the therapeutic YHEDA peptide across the BBB, the authors added the aforementioned LDLR-binding segment in ApoB-100 to the C-terminal of the synthesized therapeutic 5-YHEDA oligomer.

bs-5-YHEDA: YHEDAYHEDAYHEDAYHEDAYHEDA QSDIVAHLL

Using this method, they intended to deliver 5-YHEDA into the brains of senescent (SN) mice via LDLR-mediated endocytosis.

The SN Kunming mice exhibiting AD symptoms were divided into untreated, 5-YHEDA–treated, and bs-5- YHEDA–treated groups. Two hundred microliters of 20 mM 5-YHEDA or bs-5-YHEDA solution was intracardially injected into each mouse in the latter two groups weekly. The 6-month-old mice and the aging mice that did not display SN symptoms were used as the controls. Six weeks later, all mice underwent a 4-day MWM test after 1 day of adaptation. The path that the mouse swam to return to the underwater platform and the time spent were recorded to evaluate the individual’s cognitive ability

The results of intravenous injections of bs-5YHEDA into senescent mice demonstrated that bs-YHEDA entered the brain, increased ferriportin levels, reduced iron and free radical levels, decreased the consequences of neuronal necrosis and ameliorated cognitive disfunction without kidney or liver damage. bs-5YHEDA is a safe iron and free radical remover that potentially alleviates aging and Alzheimer's disease.

The bs-5-YHEDA–treated SN mice took only 57 seconds on average and swam 220 cm to return to the hidden platform in the MWM, nearly 25 seconds faster and 90 cm less than the untreated mice and the 5-YHEDA–treated SN mice , which suggests that the synthesized bs-5-YHEDA peptide prevented the deterioration of cognition and memory in the mice.

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An article published by Aileen l. Pogue of Alchem ​​Biotech Research in Canada and his colleagues at Louisiana State University discuss a pro-inflammatory toxin that may contribute to the development of Alzheimer's disease. The results are published in Frontiers in Neurology.

This article is (as usual) aggressively promoted, but probably not as new or important as its promoters would hope, nevertheless the subject is interesting even though it has made the subject of numerous scientific publications.

Intestinal dysbiosis has been implicated in the pathogenesis and progression of Alzheimer's disease by initiating and prolonging neuroinflammatory processes. Gut microbiota metabolites appear to be critical in the gut-brain axis mechanism. Gut microbiota metabolites, such as trimethylamine n-oxide, lipopolysaccharide, and short-chain fatty acids, are suggested to mediate systemic inflammation and intracerebral amyloidosis via endothelial dysfunction. New data suggest that the fungal microbiota may also influence the pathology of Alzheimer's disease.

Pogue and his colleagues believe they have found evidence that the lipopolysaccharide molecule in the human gastrointestinal (GI) tract generates an endotoxin which can perturb cells in the brain. Their paper links several recent observations linking lipopolysaccharide-induced increase in NF-kB signaling to increase in microRNA-30b.

NF-κB plays a key role in regulating the immune response to infection. Improper regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in synaptic plasticity and memory processes.

MicroRNAs (miRNAs) are short non-coding RNAs that are involved in post-transcriptional regulation of gene expression by affecting both stability and translation of mRNAs. MicroRNAs are thought to have regulatory roles through complementarity with mRNA. These microRNAs regulate a number of genes associated with breast cancer.

The authors show that an increase in miRNA-30b is able to decrease the expression of neuron-specific neurofilament light chain (NFL) messenger RNA in stressed human neuronal-glial cells cultures.

Neurofilaments provide structural support to axons and regulate axon diameter, which influences nerve conduction velocity. Neurofilament light chain depletion therefore disrupts the normal shape of neuronal cells, their cytoarchitecture and synaptic organization. Neurofilament light chains are a useful marker for monitoring disease in amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease, and more recently Huntington's disease.

The presence of endotoxins, when detected in the blood, is called endotoxemia. Endotoxemia is associated with obesity, diet, cardiovascular disease and diabetes.

There is experimental and observational evidence that lipopolysaccharide may play a role in depression. Administration of lipopolysaccharide in mice can lead to depressive symptoms, and there appear to be elevated levels of lipopolysaccharide in some people with depression. Inflammation can sometimes play a role in the development of depression, and lipopolysaccharide is pro-inflammatory.

Finally, lipopolysaccharide-induced inflammation can induce cellular senescence, as has been demonstrated for lung epithelial cells and microglial cells (the latter leading to neurodegeneration).

In this study, researchers detail the pathway of BF-lipopolysaccharide from the gut to the brain and its mechanisms of action once there. For them, BF-lipopolysaccharide leaks out of the gastrointestinal tract, crosses the blood-brain barrier via the circulatory system and gains access to the cerebral compartments. Next, it increases inflammation in brain cells and inhibits neuron-specific neurofilament light (NF-L), a protein that supports cellular integrity.

A deficiency of this protein leads to progressive atrophy of neuronal cells, and ultimately to cell death, as seen in neurons affected by Alzheimer's disease. They also report that an adequate intake of dietary fiber can prevent the process.

Indeed, 60% of gut microbiome variation is attributable to diet. Therefore, modulating the gut microbiome through dietary means could be an effective approach to reduce the risk of Alzheimer's disease.

Data from animal studies have suggested that dietary fat acts as the primary macronutrient responsible for postprandial endotoxemia, and that the quantity and quality of dietary fat differentially influence metabolic endotoxemia.

Additionally, healthy diets high in unsaturated fatty acids have been associated with lower circulating levels of lipopolysaccharide, which is strongly associated with lower pro-inflammatory markers. Conversely, consumption of diets high in energy or saturated fat has been associated with increased postprandial levels of lipopolysaccharide and increased circulating levels of pro-inflammatory markers.

Since people do not eat single nutrients and instead consume a diverse range of foods and a combination of nutrients that are likely to be interacting, studying the effects of whole diets offers the possibility of accounting for the interactions between different nutrients. It is also probable that introducing variety in diet helps in having a diverse microbiome. Yet has people age, digestion becomes more difficult and aging people often prefer to not change their diet.

Thus, dietary habits may be more predictive of a real effect on the gut microbiome and Alzheimer's disease risk than foods or nutrients taken in isolation.

On sait depuis 2017 que certaines personnes atteintes de diabète de type 2 ont un risque plus élevé de développer la maladie d'Alzheimer.

Une variante de l'un des principaux gènes impliqués dans la maladie d'Alzheimer: APOE4, semble interférer avec la capacité des cellules cérébrales à utiliser l'insuline, ce qui peut éventuellement provoquer le stress (en quelque sorte l'état de famine) et la mort des cellules nerveuses. Officieusement, on appelle parfois cela: Le diabète de type 3.

L'insuline régule le métabolisme des glucides, des lipides et des protéines en favorisant l'absorption du glucose du sang par le foie, les graisses et les cellules musculaires squelettiques.

Des concentrations élevées d'insuline dans le sang inhibent fortement la production et la sécrétion de glucose par le foie. L'insuline circulante affecte également la synthèse des protéines (augmentation de la masse tissulaire) dans une grande variété de tissus.

A l'inverse, de faibles niveaux d'insuline dans le sang ont l'effet inverse en favorisant un catabolisme (fonte des tissus) généralisé, en particulier de la graisse corporelle de réserve.

On pense que chez personnes diabétiques, l'utilisation ou la signalisation de l'insuline par leur cerveau ne fonctionne pas. Leur risque de développer la maladie d'Alzheimer est environ 10 à 15 fois plus élevé.

Ce nouvel article de Gemma Salvadó et ses collègues apporte davantage d'informations sur ce sujet.

L'activation gliale (les cellules nerveuses autres que les neurones) est l'un des premiers mécanismes à être altérés dans la maladie d'Alzheimer.

La protéine acide fibrillaire gliale (GFAP) est une protéine protéine de filament intermédiaire (IF) qui est exprimée par de nombreux types de cellules du système nerveux central (SNC), y compris les astrocytes.

Il existe de multiples troubles associés à une mauvaise régulation de la GFAP, et une blessure peut provoquer une réaction néfaste des cellules gliales. La cicatrisation gliale est une conséquence de plusieurs conditions neurodégénératives, ainsi que des blessures qui sectionnent le matériel neural. La cicatrice est formée par des astrocytes interagissant avec le tissu fibreux pour rétablir les marges gliales autour du noyau central de la lésion et est partiellement causée par une régulation à la hausse de la GFAP.

La protéine acide fibrillaire gliale est liée à l'astrogliose réactive (la destruction des astrocytes, des cellules nerveuses différentes des neurones) et peut être mesurée à la fois dans le liquide céphalo-rachidien et le sang.

Il a été suggéré que la GFAP plasmatique soit modifiée plus tôt dans la maladie d'Alzheimer que son homologue du liquide céphalo-rachidien.

Bien que les astrocytes consomment environ la moitié de l'énergie dérivée du glucose dans le cerveau, la relation entre l'astrogliose réactive et le métabolisme cérébral du glucose est mal comprise. Le fluorodésoxyglucose (FDG) est un analogue du glucose marqué avec un isotope émetteur de positrons (18F) qui permet de mesurer la consommation cérébrale régionale de glucose à l'aide de la tomographie par émission de positons (TEP).

Les auteurs espagnols visaient à étudier l'association entre l'absorption de fluorodésoxyglucose (FDG) et l'astrogliose réactive, au moyen de GFAP quantifié à la fois dans le plasma et le liquide céphalo-rachidien pour les mêmes participants. GFAP est une protéine de filament intermédiaire astrocytaire, principalement exprimée dans le cerveau.

La cohorte ALFA a caractérisé la maladie d'Alzheimer préclinique chez 2743 individus sans troubles cognitifs, âgés de 45 à 75 ans, et enrichie pour les antécédents familiaux de maladie d'Alzheimer sporadique. Dans cette cohorte de parents, 419 participants ALFA +  ont été sélectionnés pour être préférentiellement porteurs d'APOE-ε4 et/ou pour être des enfants adultes de patients AD. Ces participants ont subi une évaluation plus complète incluant une ponction lombaire et une TEP Aβ et [18F]FDG.

Pour cette étude, les auteurs ont inclus 314 participants sans troubles cognitifs de la cohorte ALFA+, dont 112 étaient positifs à l'amyloïde-β. Les associations entre les marqueurs GFAP et l'absorption de [18F]FDG ont été étudiées. Les auteurs ont également cherché à savoir si ces associations étaient modifiées par le statut Aβ et tau.

La GFAP plasmatique était positivement associée à la consommation de glucose dans tout le cerveau, tandis que les associations de GFAP du liquide céphalo-rachidien avec l'absorption de [18F]FDG n'ont été observées que dans des zones spécifiques plus petites comme le pôle temporal et le lobe temporal supérieur.

Ces associations ont persisté lors de la prise en compte des biomarqueurs de la pathologie Aβ, mais sont devenues négatives chez les participants Aβ-positifs et tau-positifs dans des domaines similaires de l'hypométabolisme lié à la maladie d'Alzheimer.

Une réactivité astrocytaire plus élevée, probablement en réponse aux changements pathologiques précoces de la maladie d'Alzheimer, est liée à une consommation de glucose plus élevée. Avec l'apparition de la pathologie tau, le découplage observé entre les biomarqueurs astrocytaires et la consommation de glucose pourrait indiquer une incapacité à maintenir les demandes énergétiques plus élevées requises par les astrocytes réactifs.

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It's known since some time that there is a link between blood and Alzheimer disease.

For example in 2019, after being dosed with GRF6021, a drug proposed by Alkahest, a California-based startup, Alzheimer's patients in a clinical trial retained memory and mental function for six months - when they would normally be expected to deteriorate. GRF6021, a drug proposed by Alkahest, a California-based startup, is made from the blood of young people.

On contrary a large study found that people who experienced a blood transfusion may be at risk of Alzheimer's disease or may be, because they were transfused with "old blood".

A research team led by Claudio Soto, in the Department of Neurology with McGovern Medical School at UTHealth Houston, with Akihiko Urayama, as first author, performed a series of whole blood exchange treatments to partially replace blood from mice exhibiting Alzheimer's disease-causing amyloid precursor proteins with complete blood from healthy mice of the same genetic background.

The results of the study was published in Molecular Psychiatry.

The development of cerebral amyloid plaques in a transgenic mice model of AD (Tg2576) was significantly reduced by 40–80% through exchanging whole blood with normal blood from wild type mice having the same genetic background. Importantly, such reduction resulted in improvement in spatial memory performance in aged Tg2576 mice.

The exact mechanism by which blood exchange reduces amyloid pathology and improves memory is presently unknown, but measurements of Aβ in plasma soon after blood exchange suggest that mobilization of Aβ from the brain to blood may be implicated.

Their results suggest that a target for AD therapy may exist in the peripheral circulation, which could open a novel disease-modifying intervention for AD. Technologies commonly used in medical practice, such as plasmapheresis or blood dialysis, could 'clean' blood from Alzheimer's patients, reducing the buildup of toxic substances in the brain.

This was suggested recently.