SENS Research Foundation is delighted to announce a matching grant from the Antonov Foundation. The Antonov Foundation will match every donation between now and the end of the campaign on December 31, 2020 - up to a total of 600,000!

SENS Research Foundation is incredibly grateful for this generous investment in the future we all hope to create - a future where getting older brings wisdom and experience but not disease, suffering, and pain. Thank you, Michael Antonov, and thank you to all who have donated so far to our end of year campaign. And if you're still planning on donating, there's no better time to do it than on Giving Tuesday this December 1!

Michael Antonov said: "I've followed and supported SENS research over the last few years and am excited to up my commitment this year because their organized, practical approach to combating aspects of aging, such as breaking down of cross-links, rejuvenating the mitochondria, and clearance of senescent cells has potential to help human lives and achieve age reversal in the near future."

Glycation is a non-enzymatic chemical reaction that occurs between a ketone or aldehyde group of fructose or glucose and an amino acid residue or the hydroxy-group of a protein or lipid, and is often referred to as the Maillard reaction. Protein glycation occurs through a complex series of very slow reactions in the body, including the formation of the stable Amadori-lysine products (Schiff bases). These give rise to advanced glycation end-products (AGEs).

It is hypothesized that the production and accumulation of AGEs have causal roles in the development of the complications associated with aging and lifestyle-related diseases, such as diabetes, atherosclerosis, and hyperlipidemia. Furthermore, the production and accumulation of AGEs are involved in the development of other diseases, such as cardiovascular diseases, cerebrovascular disorders, chronic renal failure, Alzheimer's disease, and Parkinson's disease. Therefore, the identification of safe treatments that can inhibit glycation is required, as they may exhibit anti-aging effects, or serve as a therapeutic option for prevention of diseases associated with glycation.

In the present study, the ability of sodium 4-phenylbutyrate (PBA) on inhibition of glycation was assessed. In vitro, PBA inhibited the glycation of albumin and collagen by up to 42.1% and 36.9%, respectively. Furthermore, when spontaneously diabetic KK mice were administered PBA (20 mg/day) or vehicle orally, glycosuria developed rapidly in the control mice, but after 6 weeks, only one treated mouse was glycosuric. In addition, the weight gain and HbA1c levels were significantly lower in the treated mice compared with the untreated mice. These results suggested that PBA also inhibited glycation in vivo. Further studies are required to determine whether PBA may be effective for the therapy or prevention of aging or lifestyle-related diseases caused by the accumulation of AGEs. The method of administration and the side-effects of PBA have already been established as PBA is already used clinically. Therefore, the repurposing of PBA for reducing AGE levels may be a potential option to reduce complications associated with aging.

Age-related pathologies are a major global disease burden, with potentially half of all morbidities being attributable to aging. Inflammation (or "inflammaging") is one of the main causative factors contributing to disease progression, and has been described in various age-related pathologies, including type 2 diabetes (T2D) and cardiovascular disease. While being beneficial in the acute stages of an insult, inflammation increasingly fails to resolve with age, leading to changes in both cellular phenotypes and immune system composition. Senescence pathways are induced by, as well as potentiate, chronic inflammation, with increased cellular senescence being observed in various age-related diseases. Cellular senescence is characterized by a stable growth arrest and a proinflammatory secretome, which potentiates low grade chronic inflammation, thereby building a positive feedback loop, gradually exacerbating its effects on the body.

With a prevalence of approximately 44% in the elderly population (of 65 years and older), chronic kidney disease (CKD) presents a major disease burden in an aging population. Therapies for late stage CKD including dialysis and renal transplantation carry a significant burden for patients, and the outcome is often poor; therefore, there is a significant need for early diagnosis and novel therapies targeting mechanisms driving the disease. CKD is associated with chronic inflammation, elevated levels of cellular senescence, as well as immune system dysfunction.

Senescent cells may both be a phenotype of age-related inflammatory disease, as well as the cause for disease progression. Thereby two models of disease progression exist: One in which senescent cells arise from local tissue injury, promoting senescence in neighboring cells in a paracrine manner. Alternatively, immune clearance may be impaired, thereby allowing the accumulation of senescent cells. Distinguishing between these two models becomes pivotal when exploring potential new treatments of CKD.

Much of the immune dysregulation is governed by the presence of proinflammatory cytokines, and uremia, or by pre-existing comorbidities such as high blood pressure or diabetes. In addition to the levels of inflammatory markers, an elevated white blood cell count is predictive of CKD development. This suggests various modes of pathogenesis, with the immune system, senescence, and inflammation at its core. Cellular senescence and immunosurveillance occur in conjunction, increased cellular senescence due to chronic inflammation increases the demand for immune clearance; however, as described above, uremia and inflammation lead to dysfunction of the immune system, thereby establishing a positive feedback loop in which more senescent cells drive inflammation and immune dysregulation which, in turn, cause more senescence.

Mitochondria are essential for respiration and the regulation of diverse cellular processes; thus, mitochondrial dysfunction is believed to underlie a variety of metabolic and aging-related diseases. Mutations in the mitochondrial genome are thought to drive mitochondrial dysfunction and have been implicated in aging-related diseases; however, whether mtDNA mutations are causal or consequent of metabolic dysfunction remains unclear. The polymerase gamma (PolG) "mutator" mouse is a model of intrinsic mitochondrial dysfunction and was employed for this study to determine whether mtDNA mutations are sufficient to drive metabolic abnormalities and aging-associated insulin resistance and adiposity.

Mice harboring a homozygous PolG loss of proofreading 3′-5′ exonuclease function mutation (PolGmut/mut) develop mtDNA point mutations at a rate that far exceeds mutations observed in aged wild-type (WT) animals and humans. The mtDNA point mutations that accumulate in young PolGmut/mut mice (~136-fold increase versus WT mice) manifest a variety of preadolescent phenotypic abnormalities including progeroid-like symptoms throughout maturation as well as premature death (~12-16 months of age). Because of the complexity of the early-onset aging, we studied the PolG heterozygous (PolG+/mut) mouse, which lacks progeroid-like symptoms despite a supraphysiological mtDNA point mutation frequency (~30-fold greater mutation load in PolG+/mut versus WT mice). Furthermore, male and female PolG+/mut mice show no significant difference in lifespan versus WT animals (tested up to 800 days of age).

Based on previous reports, we hypothesized that an increased mtDNA point mutation frequency in PolG+/mut mice would promote mitochondrial dysfunction and accelerate the development of insulin resistance during aging. We examined specific aspects of metabolism in male PolG+/mut mice at 6 and 12 months of age under three dietary conditions: normal chow (NC) feeding, high-fat feeding (HFD), and 24-hr starvation. We performed mitochondrial proteomics and assessed dynamics and quality control signaling in muscle and liver to determine whether mitochondria respond to mtDNA point mutations by altering morphology and turnover. In the current study, we observed that the accumulation of mtDNA point mutations failed to disrupt metabolic homeostasis and insulin action in male mice, but with aging, metabolic health was likely preserved by countermeasures against oxidative stress and compensation by the mitochondrial proteome.

The rate of synthesis of transthyretin (TTR) is constant. For proteostasis, the rate of removal of TTR must equal the rate of synthesis. TTR in plasma is largely in the tetrameric form, (TTR)4, but dissociates to give very low, but significant concentrations of dimers and monomers. Removal of TTR from plasma proceeds via monomers.

Monomers undergo two processes that remove them from solution, proteolysis or aggregation. The combined rates of these two pathways equals the total rate of monomer removal, which is also equal to the rate of production of monomer via dissociation of tetramer. Depending on the relative rates, either of the two reaction pathways could account for anywhere from 100% to 0% of the rate of monomer removal. The critical monomer concentration for aggregation is unknown, however the cause of aggregation develops slowly over time. Once amyloidosis begins, the rate of development of amyloidosis is determined by the rate of monomer incorporation into various aggregates that lead to fibrils and amyloids.

Destabilizing tetramer by pleiotropic mutations leads to greater dissociation of monomer and a higher, variant-dependent concentration of TTR monomer in plasma. Mutations are not required for TTR amyloidosis formation; point mutations only modify the equilibrium concentrations. Amyloidosis caused by wild-type TTR follows the same mechanism as amyloidosis caused by variants of TTR and thus should be considered as variants of the same disease for purposes of clinical studies.

Amyloidosis begins when the rate of TTR proteolysis decreases relative to the rate of amyloid formation and monomer concentration increases sufficiently to allow significant oligomerization into fibrils and amyloids. The cause of a decrease in the rate of proteolysis of TTR remains to be identified. When the tetramer is stabilized by drugs or stabilizing mutations, the concentration of tetramer will increase in plasma to a steady-state level determined by the rate of proteolysis.

Researchers studied the enzyme Tsa1, which is part of a group of antioxidants called peroxiredoxins. Previous studies of these enzymes have shown that they participate in yeast cells' defences against harmful oxidants. But the peroxiredoxins also help extend the life span of cells when they are subjected to calorie restriction. The mechanisms behind these functions have not yet been fully understood.

It is already known that reduced calorie intake can significantly extend the life span of a variety of organisms, from yeast to monkeys. Several research groups have also shown that stimulation of peroxiredoxin activity in particular is what slows down the ageing of cells, in organisms such as yeast, flies, and worms, when they receive fewer calories than normal through their food. "Now we have found a new function of Tsa. Previously, we thought that this enzyme simply neutralises reactive oxygen species. But now we have shown that Tsa1 actually requires a certain amount of hydrogen peroxide to be triggered to participate in the process of slowing down the ageing of yeast cells."

Surprisingly, the study shows that Tsa1 does not affect the levels of hydrogen peroxide in aged yeast cells. On the contrary, Tsa1 uses small amounts of hydrogen peroxide to reduce the activity of a central signalling pathway when cells are getting fewer calories. The effects of this ultimately lead to a slowdown in cell division and processes linked to the formation of the cells' building blocks. The cells' defences against stress are also stimulated - which causes them to age more slowly.

Intestinal bacteria can influence the functioning of the brain and promote neurodegeneration through several pathways: they can indeed influence the regulation of the immune system and, consequently, can modify the interaction between the immune system and the nervous system. Lipopolysaccharides, a protein located on the membrane of bacteria with pro-inflammatory properties, have been found in amyloid plaques and around vessels in the brains of people with Alzheimer's disease. In addition, the intestinal microbiota produces metabolites - in particular some short-chain fatty acids - which, having neuroprotective and anti-inflammatory properties, directly or indirectly affect brain function.

"To determine whether inflammation mediators and bacterial metabolites constitute a link between the gut microbiota and amyloid pathology in Alzheimer's disease, we studied a cohort of 89 people between 65 and 85 years of age. Some suffered from Alzheimer's disease or other neurodegenerative diseases causing similar memory problems, while others did not have any memory problems. Using PET imaging, we measured their amyloid deposition and then quantified the presence in their blood of various inflammation markers and proteins produced by intestinal bacteria, such as lipopolysaccharides and short-chain fatty acids."

This work thus provides proof of an association between certain proteins of the gut microbiota and cerebral amyloidosis through a blood inflammatory phenomenon. Scientists will now work to identify specific bacteria, or a group of bacteria, involved in this phenomenon. This discovery paves the way for potentially highly innovative protective strategies - through the administration of a bacterial cocktail, for example, or of prebiotics to feed the "good" bacteria in our intestine.

Injuries in the central nervous system (CNS) often causes neuronal loss and glial scar formation. We have recently demonstrated NeuroD1-mediated direct conversion of reactive glial cells into functional neurons in adult mouse brains. Here, we further investigate whether such direct glia-to-neuron conversion technology can reverse glial scar back to neural tissue in a severe stab injury model of the mouse cortex. Using an adeno-associated virus (AAV)-based gene therapy approach, we ectopically expressed a single neural transcription factor NeuroD1 in reactive astrocytes in the injured areas.

We discovered that the reactive astrocytes were efficiently converted into neurons both before and after glial scar formation, and the remaining astrocytes proliferated to repopulate themselves. The astrocyte-converted neurons were highly functional, capable of firing action potentials and establishing synaptic connections with other neurons. Unexpectedly, the expression of NeuroD1 in reactive astrocytes resulted in a significant reduction of toxic A1 astrocytes, together with a significant decrease of reactive microglia and neuroinflammation. Furthermore, accompanying the regeneration of new neurons and repopulation of new astrocytes, new blood vessels emerged and blood-brain-barrier (BBB) was restored. These results demonstrate an innovative neuroregenerative gene therapy that can directly reverse glial scar back to neural tissue, opening a new avenue for brain repair after injury.

Cellular senescence is a phenomenon that has been known about for a long time. During recent years, it has gained growing interest as its causal involvement in the aging process has been corroborated by several experimental findings. Because of this, several groups and companies are developing senolytic approaches that aim to remove senescent cells from aged animals in the hope of achieving a rejuvenation and life extension effect. However, at the same time, cellular senescence is also seen as an anti-cancer strategy, which raises the question why interfering with an anti-cancer mechanism should increase life span?

The argument that antagonistic pleiotropy explains the anti-tumorigenic as well as the pro-tumorigenic and inflammatory properties of senescent cells is problematic, since there are multiple ways imaginable to break the link between positive and negative effects. In this paper, we discussed an alternative idea for the evolution of cellular senescence that focuses on the involvement of senescent cells in the repair of cell and tissue damage. From such a viewpoint, many properties of the SASP make much more sense and are actually beneficial. Additionally, the recent finding that also post-mitotic cells can display characteristics of cellular senescence, agrees well with this idea. While post-mitotic cells benefit from triggering a healing and repair mechanism, they do not profit from an anti-cancer process.

According to our interpretation, the negative effects of cellular senescence only emerge because the clearance of senescent cells by the immune system, once the repair process has finished, is imperfect. Senescent cells represent a very heterogeneous population, depending on the original cell type and on how senescence was triggered. We therefore proposed that there is a continuum of turnover rates, since the immune system is more or less capable of recognizing this range of subtypes. A mathematical model, which for simplicity only uses two types of senescent cells (removable and non-removable), achieves an excellent fit to experimental data. Interestingly, our model also predicts a slowdown of senescent cell turnover with age, in our case explained by an accumulation of non-removable senescent cells relative to removable ones.

For obvious reasons, there are high hurdles for the destruction of body cells. We propose that for this reason, the optimal strategy is for the immune system to accept a small fraction of false negatives, leading to the slow accumulation of senescent cells in the body. This, in turn, then leads to life-threatening consequences like chronic inflammation (inflammaging), degenerative diseases, and cancer. In this interpretation of cellular senescence, there needs to be a balance between beneficial effects (i.e., wound healing and tissue repair) and negative consequences (i.e., accumulation of senescent cells with inflammation and diseases).

To see how this differs from the idea that cellular senescence is an anti-cancer strategy, we have to return to the questions that we posed earlier. Why did evolution not break the connection of the antagonistic effects and why do organisms not rely exclusively on apoptosis as anti-cancer strategy? The discussed proposal makes it more difficult to break the antagonistic effects, since there is always a trade-off between overlooking too many senescent cells (false negatives) and killing too many healthy body cells (false positives). However, the situation can be improved quantitatively by somehow enabling the immune system to better recognize senescent cells. Indeed, it may be that this has already happened during the evolution of long-lived species, which accumulate senescent cells at a slower pace than short-lived species.

If this outline of the evolution of cellular senescence is correct, it also follows that the removal of accumulated senescent cells is a good strategy, as long as it does not interfere with the primary function of this process. Thus, a brief senolytic treatment would be suitable, while a chronically administered drug might be problematic.

Parabiosis studies have yielded a plethora of insights regarding mechanisms that underlie the aging of stem cell niches. It was shown that old partners have better health in multiple tissues when they shared blood with a younger animal. A prominent interpretation of heterochronic parabiosis is that aging is malleable and that the aging process can be slowed or even reversed. Brain aging in particular is associated with a progressive loss of functionality and is thought to be in large part the result of an excessive activation of microglia, the brain-resident myeloid cells. The age-related declines in brain function and cognition (among many other functions in the body) were once considered inevitable and permanent. Parabiosis studies, interestingly, have challenged this notion by illustrating the plasticity of brain maintenance and function after changing the age of the blood.

Several systemic proteins and young plasma infusions were suggested to influence the plasticity of brain aging, albeit with some controversy to the actual age-specific levels of some of these candidate factors, such as GDF11, B2M, CCL11, and TIMP2. There was also a lack of health span increase in young plasma infusion studies; and while safety trials were successful, the young blood approaches have not been demonstrated to be effective in improving the health of the brain or any other tissue in clinic. In concert, heterochronic blood transfusion exchange experiments have shown that in the absence of the organ sharing and environmental enrichment of parabiosis, young blood does not rejuvenate the old brain.

As we investigate and form an evolutionary conserved paradigm of systemic rejuvenation, our data demonstrated that young blood is not the primary determinant, and instead, dilution of old blood plasma yields a robust resetting of the systemic signaling milieu to youth and health, rejuvenating multiple tissues. The study of the brain in that report was limited to hippocampal neurogenesis; here we expand the work to other important facets of brain health: neuroinflammation and cognition. Our data demonstrate that neuroinflammation (specifically the activation of microglia), declines and the cognitive capacity of old mice, improves after a single treatment of blood dilution. Considering that therapeutic plasma exchange (TPE) is FDA approved, this study suggests a use of this procedure to prevent, attenuate, and possibly even reverse the degenerative and inflammatory diseases of the brain.

Tau tangles are an integral part of Alzheimer's disease (AD) pathology, appearing in the hippocampus in early stage disease and then gradually spreading throughout the brain. Their accumulation closely mirrors cognitive decline. Researchers have focused on tau's role in neuron dysfunction and death. What about other cells? Researchers looked for tau tangles in different areas of the hippocampus in tissue samples from healthy controls and from people with AD. As expected, they found them in the AD samples, but the pathology was not equally distributed; there were hot spots in certain areas, including the hilus. "The hilus is seen as a highway between the dentate gyrus and CA3 region within the hippocampus, so most researchers do not pay much attention to what happens there. It turns out to be very important."

Zooming in on the astrocytes in the hilus, researchers saw they were packed with three-repeat (3R) tau in the AD tissue samples. This isoform contributes to the 3R/4R type of neurofibrillary tangles found in Alzheimer's. The amount of 3R tau in the astrocytes correlated with tau tangles and with amyloid-β plaques in the surrounding tissue, suggesting the 3R tau accumulation may be downstream of other AD pathologies. Oddly enough, researchers found no increase in phosphorylated forms of tau in the astrocytes or any evidence of tangles in these cells. He speculated that this might be because these hilar astrocytes cells do not phosphorylate the protein as easily as neurons do, or that tau is dephosphorylated by the astrocytes.

Does this 3R tau accumulation affect the astrocytes or their surrounding neurons? To test this idea in a mouse model, researchers overproduced tau in mouse hippocampi. Researchers injected lentiviruses carrying a gene for human 3R tau into the hippocampi of 3-month-old wild-type mice. Two weeks later, they verified that the human 3R tau was expressed only in hilar astrocytes. Within these astrocytes, mitochondria languished in the cell bodies, rather than travelling to the astrocyte arms that support neurons. Mitochondrial function also suffered; the organelles replenished less often, and they produced much less ATP than usual.

Still, neurons looked normal for the most part, with no signs of neuronal death. However, neurogenesis had faltered, and the treated mice had fewer parvalbumin-positive inhibitory neurons in the dentate gyrus than controls. The number of inhibitory synapses also collapsed. Parvalbumin-producing neurons are like the pacemakers of the brain, modulating γ-frequency oscillations, which is important for working memory. Indeed, the 3R mice had weaker γ activity in the hippocampus and had trouble finding a hidden platform in a water maze. Otherwise, they seemed to behave normally. Taken together, the results suggested that accumulation of tau in hilar astrocytes compromised the function of hippocampal inhibitory neurons.

As we age, we accumulate cells in many organs that exhibit signs of DNA damage, have poor proliferative capacity, and are highly secretory. These cells are senescent, defined as being in a state of cell cycle arrest associated with phenotypic and functional changes. While transient senescence is a beneficial mechanism earlier in life, the accumulation of senescent cells with increasing age leads to organ dysfunction, driving inflammation and may underlie many age-related diseases such as atherosclerosis, osteoarthritis, neurodegenerative diseases, and cirrhosis.

While senescence was first discovered in fibroblasts and extensively worked on in other non-leukocytic cells, it has become increasingly clear that immune cells undergo senescence as well. Within the immune system, the existence of non-proliferative leukocyte populations that have high capacity for biologically active mediator secretion has been recognized for many decades, albeit under a different name. These are the effector T lymphocytes that secrete pro-inflammatory cytokines and cytotoxic granules but do not proliferate after activation. Recent studies show that these cells also harbour DNA damage, short telomeres, low telomerase activity, and engage signalling pathways associated with cellular senescence. Therefore, the terms effector T cells and senescent T cells may be synonymous and refer to the same T cell populations.

The extent of T cell proliferation the acute phase of a viral infection drives T cells to senescence. These cells are still susceptible to apotosis but can persist given sufficient antiapototic cytokines in tissue niches. It can be argued that senescent T cells derive from a subpopulation of effector T cells that do not undergo apoptosis, instead becoming senescent and lingering long term. In this article we discuss data on T cell senescence, how it is regulated and evidence for novel functional attributes of senescent T cells. We discuss an interactive loop between senescent T cells and senescent non-lymphoid cells and conclude that in situations of intense inflammation, senescent cells may damage healthy tissue. While the example for immunopathology induced by senescent cells that we highlight is cutaneous leishmaniasis, this situation of organ damage may apply to other infections, including COVID-19 and also rheumatoid arthritis, where ageing, inflammation and senescent cells are all part of the same equation.

Cardiovascular disease is the leading cause of mortality and ischemic heart disease is a major cause of death worldwide. Coronary vessels that nourish the heart develop from three main sources, the endocardium on the inner surface of the hearts blood-filled chambers being one of the major contributors. In normal conditions, the adult heart can no longer generate new blood vessels from the endocardium, because the endocardium-to-coronary vessel transition is blocked by a connective tissue wall beneath the endocardium.

In a recently published study researchers show that the VEGF-B growth factor can be used to activate the growth of vessels inside of the heart during cardiac ischemic damage. This novel finding opens the possibility that vessels emerging from the inner side of the heart could be further developed for the treatment of myocardial infarction, which results from insufficient delivery of oxygen to cardiac tissue. In normal conditions, blood nourishes the adult heart through coronary vessels.

VEGF-B (vascular endothelial growth factor) belongs to a family of growth factors that regulate the formation of blood- and lymphatic vessels. Earlier attempts to utilize another growth factor gene, VEGF-A, to grow new vessels in the heart have failed, mostly due to the leakiness of the vessels and increased inflammation caused by VEGF-A, but not by VEGF-B. Re-activation of the embryonic vessel growth program in adult endocardium could be a new therapeutic strategy for cardiac neovascularization after myocardial infarction. For possible future clinical use, the function of these vessels and their blood flow has to be further studied to ensure that they really increase transport of oxygen and nutrients into the cardiac muscle.

The aging process is characterized by the presence of high interindividual variation between individuals of the same chronical age prompting a search for biomarkers that capture this heterogeneity. Epigenetic clocks measure changes in DNA methylation levels at specific CpG sites that are highly correlated with calendar age. The discrepancy resulting from the regression of DNA methylation age on calendar age is hypothesised to represent a measure of biological ageing with a positive or negative residual signifying age acceleration or deceleration respectively.

The present study examines the associations of four epigenetic clocks - Horvath, Hannum, PhenoAge, GrimAge - with a wide range of clinical phenotypes (walking speed, grip strength, Fried frailty, polypharmacy, Mini-Mental State Exam (MMSE), Montreal Cognitive Assessment (MOCA), Sustained Attention Reaction Time, 2-choice reaction time), and with all-cause mortality at up to 10-year follow-up, in a sample of 490 participants in the Irish Longitudinal Study on Ageing (TILDA).

Horvath Age Acceleration (AA) and HannumAA were not predictive of health; PhenoAgeAA was associated with 4 of 9 outcomes (walking speed, frailty, MOCA, MMSE) in minimally adjusted models, but not when adjusted for other social and lifestyle factors. GrimAgeAA by contrast was associated with 8 of 9 outcomes (all except grip strength) in minimally adjusted models, and remained a significant predictor of polypharmacy, frailty, and mortality in fully adjusted models. Results indicate that the GrimAge clock represents a step-improvement in the predictive utility of the epigenetic clocks for identifying age-related decline in an array of clinical phenotypes promising to advance precision medicine.

Researchers have identified certain regions in the retina - the lining found in the back of the eye - that are more affected by Alzheimer's disease than other areas. The findings were from a clinical trial involving people older than 40 who were showing signs of cognitive decline. In the trial, investigators used a noninvasive technique known as sectoral retinal amyloid imaging to capture retinal images in participants. The retina, which is directly connected to the brain, is the only central nervous system tissue accessible for patient-friendly, high-resolution and noninvasive imaging.

The images were then analyzed using a new process that could identify certain peripheral regions in the retina that corresponded better to brain damage and cognitive status. In studying the images, scientists could detect patients with an increased buildup of retinal amyloid protein, signifying a higher likelihood of developing Alzheimer's disease or cognitive impairments. These findings build upon pioneering research in 2010 in which researchers identified a pathological hallmark of Alzheimer's disease, amyloid beta-protein deposits, in retinal tissues from deceased patients. The team then developed a methodology to detect retinal amyloid beta-protein plaques in living patients suffering from the disease.