1. Blueberry vinegar improves memory in mice with amnesia

    January 9, 2018 by Ashley

    From the American Chemical Society press release:

    Dementia affects millions of people worldwide, robbing them of their ability to think, remember and live as they once did. In the search for new ways to fight cognitive decline, scientists report in ACS’ Journal of Agricultural and Food Chemistry that blueberry vinegar might offer some help. They found that the fermented product could restore cognitive function in mice.

    Recent studies have shown that the brains of people with Alzheimer’s disease, the most common form of dementia, have lower levels of the signaling compound acetylcholine and its receptors. Research has also demonstrated that blocking acetylcholine receptors disrupts learning and memory. Drugs to stop the breakdown of acetylcholine have been developed to fight dementia, but they often don’t last long in the body and can be toxic to the liver. Natural extracts could be a safer treatment option, and some animal studies suggest that these extracts can improve cognition. Additionally, fermentation can boost the bioactivity of some natural products. So Beong-Ou Lim and colleagues wanted to test whether vinegar made from blueberries, which are packed with a wide range of active compounds, might help prevent cognitive decline.

    To carry out their experiment, the researchers administered blueberry vinegar to mice with induced amnesia. Measurements of molecules in their brains showed that the vinegar reduced the breakdown of acetylcholine and boosted levels of brain-derived neurotrophic factor, a protein associated with maintaining and creating healthy neurons. To test how the treatment affected cognition, the researchers analyzed the animals’ performance in mazes and an avoidance test, in which the mice would receive a low-intensity shock in one of two chambers. The treated rodents showed improved performance in both of these tests, suggesting that the fermented product improved short-term memory. Thus, although further testing is needed, the researchers say that blueberry vinegar could potentially be a promising food to help treat amnesia and cognitive decline related to aging.


  2. First brain training exercise positively linked to dementia prevention identified

    December 19, 2017 by Ashley

    From the Indiana University press release:

    Aging research specialists have identified, for the first time, a form of mental exercise that can reduce the risk of dementia.

    The cognitive training, called speed of processing, showed benefits up to 10 years after study participants underwent the mental exercise program, said Frederick W. Unverzagt, PhD, professor of psychiatry at Indiana University School of Medicine.

    The proportion of participants who underwent the training and later developed dementia was significantly smaller than among those who received no cognitive training, the researchers said.

    There were measurable benefits even though the amount of training was small and spread out over time: 10 one-hour sessions over six weeks initially and up to eight booster sessions after that.

    “We would consider this a relatively small dose of training, a low intensity intervention. The persistence — the durability of the effect was impressive,” said Dr. Unverzagt, who explains more in a Q&A blog post.

    Results from the Advanced Cognitive Training in Vital Elderly — ACTIVE — study of 2,802 older adults were recently reported in Alzheimer & Dementia Translational Research and Clinical Interventions, a peer-reviewed journal of the Alzheimer’s Association.

    The researchers, from IU, the University of South Florida, Pennsylvania State University and Moderna Therapeutics, examined healthy adults aged 65 years and older from multiple sites and who were randomly assigned to one of four treatment groups:

    • Participants who received instructions and practice in strategies to improve memory of life events and activities.
    • Participants who received instruction and practice in strategies to help with problem solving and related issues.
    • Participants who received computer-based speed of processing exercises — exercises designed to increase the amount and complexity of information they could process quickly.
    • A control group whose members did not participate in any cognitive training program.

    Initial training consisted of 10 sessions lasting about an hour, over a period of five to six weeks. A subset of participants who completed least 80 percent of the first round of training sessions were eligible to receive booster training, which consisted of four 60 to 75-minute sessions 11 months and 35 months following the initial training. Participants were assessed immediately after training and at one, two, three, five and 10 years after training.

    After attrition due to death and other factors, 1,220 participants completed the 10-year follow-up assessment. During that time, 260 participants developed dementia. The risk of developing dementia was 29 percent lower for participants in speed of processing training than for those who were in the control group, a statistically significant difference. Moreover, the benefits of the training were stronger for those who underwent booster training. While the memory and reasoning training also showed benefits for reducing dementia risk, the results were not statistically significant.

    Dr. Unverzagt noted that the speed of processing training used computerized “adaptive training” software with touch screens. Participants were asked to identify objects in the center of the screen, while also identifying the location of briefly appearing objects in the periphery. The software would adjust the speed and difficulty of the exercises based on how well participants performed.

    In contrast the memory and reasoning programs used more traditional instruction and practice techniques as might occur in a classroom setting.

    Earlier studies had shown that ACTIVE cognitive training improved participants’ cognitive abilities and the ease of engaging in activities of daily living five and 10 years after the initial training. However, an examination of the role of ACTIVE cognitive training on dementia incidence was not significant after five years of follow-up.


  3. Study links canola oil to worsened memory and learning ability in Alzheimer’s

    December 17, 2017 by Ashley

    From the Temple University Health System press release:

    Canola oil is one of the most widely consumed vegetable oils in the world, yet surprisingly little is known about its effects on health. Now, a new study published online December 7 in the journal Scientific Reports by researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) associates the consumption of canola oil in the diet with worsened memory, worsened learning ability and weight gain in mice which model Alzheimer’s disease. The study is the first to suggest that canola oil is more harmful than healthful for the brain.

    “Canola oil is appealing because it is less expensive than other vegetable oils, and it is advertised as being healthy,” explained Domenico Praticò, MD, Professor in the Departments of Pharmacology and Microbiology and Director of the Alzheimer’s Center at LKSOM, as well as senior investigator on the study. “Very few studies, however, have examined that claim, especially in terms of the brain.”

    Curious about how canola oil affects brain function, Dr. Praticò and Elisabetta Lauretti, a graduate student in Dr. Pratico’s laboratory at LKSOM and co-author on the new study, focused their work on memory impairment and the formation of amyloid plaques and neurofibrillary tangles in an Alzheimer’s disease mouse model. Amyloid plaques and phosphorylated tau, which is responsible for the formation of tau neurofibrillary tangles, contribute to neuronal dysfunction and degeneration and memory loss in Alzheimer’s disease. The animal model was designed to recapitulate Alzheimer’s in humans, progressing from an asymptomatic phase in early life to full-blown disease in aged animals.

    Dr. Praticò and Lauretti had previously used the same mouse model in an investigation of olive oil, the results of which were published earlier in 2017. In that study, they found that Alzheimer mice fed a diet enriched with extra-virgin olive oil had reduced levels of amyloid plaques and phosphorylated tau and experienced memory improvement. For their latest work, they wanted to determine whether canola oil is similarly beneficial for the brain.

    The researchers started by dividing the mice into two groups at six months of age, before the animals developed signs of Alzheimer’s disease. One group was fed a normal diet, while the other was fed a diet supplemented with the equivalent of about two tablespoons of canola oil daily.

    The researchers then assessed the animals at 12 months. One of the first differences observed was in body weight — animals on the canola oil-enriched diet weighed significantly more than mice on the regular diet. Maze tests to assess working memory, short-term memory, and learning ability uncovered additional differences. Most significantly, mice that had consumed canola oil over a period of six months suffered impairments in working memory.

    Examination of brain tissue from the two groups of mice revealed that canola oil-treated animals had greatly reduced levels of amyloid beta 1-40. Amyloid beta 1-40 is the more soluble form of the amyloid beta proteins. It generally is considered to serve a beneficial role in the brain and acts as a buffer for the more harmful insoluble form, amyloid beta 1-42.

    As a result of decreased amyloid beta 1-40, animals on the canola oil diet further showed increased formation of amyloid plaques in the brain, with neurons engulfed in amyloid beta 1-42. The damage was accompanied by a significant decrease in the number of contacts between neurons, indicative of extensive synapse injury. Synapses, the areas where neurons come into contact with one another, play a central role in memory formation and retrieval.


  4. PET tracer gauges effectiveness of promising Alzheimer’s treatment

    by Ashley

    From the Society of Nuclear Medicine and Molecular Imaging press release:

    In the December featured basic science article in The Journal of Nuclear Medicine, Belgian researchers report on the first large-scale longitudinal imaging study to evaluate BACE1 inhibition with micro-PET in mouse models of Alzheimer’s disease. PET imaging has been established as an excellent identifier of the amyloid plaque and tau tangles that characterize Alzheimer’s disease. Now it is proving to be an effective way to gauge treatment effectiveness.

    The tracer makes it possible to image the effects of chronic administration of an inhibitor for an enzyme, called beta (?)-site amyloid precursor protein-cleaving enzyme 1 (BACE1), which cuts off protein fragments that can lead to amyloid-? development and is more prevalent in brains affected by Alzheimer’s. It does this by binding to BACE1.

    The study compared control mice with those genetically-altered to have Alzheimer’s, and tested 18F-florbetapir (18F-AV45) along with two other tracers, 18F-FDG PET and 18F-PBR111. The mice received the BACE inhibitor at 7 weeks, then brain metabolism, neuroinflammation and amyloid-? pathology were measured using a micro-PET (?PET) scanner and each of the tracers. Baseline scans were done at 6-7 weeks and follow-up scans at 4,7 and 12 months. 18F-AV45 uptake was measured at 8 and 13 months of age. After the final scans, microscopic studies were performed.

    While all three tracers detected pathological differences between the genetically modified mice and the controls, only 18F-AV45 showed the effects of inhibitor treatment by identifying reduced amyloid-? pathology in the genetically modified mice. This was confirmed in the microscopic studies.

    The team of the Molecular Imaging Center Antwerp, Belgium, however warns, “This study clearly showed that accurate quantification of amyloid-beta tracers is critically important and that the non-specific uptake in the brain of subjects might be underestimated for some existing Alzheimer’s tracers that have fast metabolization profiles. The aim of this translational research is advancing results discovered at the bench so that they can be applied to patients at the bedside.”

    The statistics on Alzheimer’s are sobering. Approximately 10 percent of people 65 and older have Alzheimer’s dementia, according to the Alzheimer’s Association. More than 5 million Americans are living with the disease, and that number could rise to 16 million by 2050.


  5. Study suggests some video games are good for older adults’ brains

    December 15, 2017 by Ashley

    From the Université de Montréal press release:

    If you’re between 55 and 75 years old, you may want to try playing 3D platform games like Super Mario 64 to stave off mild cognitive impairment and perhaps even prevent Alzheimer’s disease.

    That’s the finding of a new Canadian study by Université de Montréal psychology professors Gregory West, Sylvie Belleville and Isabelle Peretz. Published in PLOS ONE, it was done in cooperation with the Institut universitaire de gériatrie de Montréal (IUGM), Benjamin Rich Zendel of Memorial University in Newfoundland, and Véronique Bohbot of Montreal’s Douglas Hospital Research Centre.

    In two separate studies, in 2014 and 2017, young adults in their twenties were asked to play 3D video games of logic and puzzles on platforms like Super Mario 64. Findings showed that the gray matter in their hippocampus increased after training.

    The hippocampus is the region of the brain primarily associated with spatial and episodic memory, a key factor in long-term cognitive health. The gray matter it contains acts as a marker for neurological disorders that can occur over time, including mild cognitive impairment and Alzheimer’s.

    West and his colleagues wanted to see if the results could be replicated among healthy seniors.

    The research team recruited 33 people, ages 55 to 75, who were randomly assigned to three separate groups. Participants were instructed to play Super Mario 64 for 30 minutes a day, five days a week, take piano lessons (for the first time in their life) with the same frequency and in the same sequence, or not perform any particular task.

    The experiment lasted six months and was conducted in the participants’ homes, where the consoles and pianos, provided by West’s team, were installed.

    The researchers evaluated the effects of the experiment at the beginning and at the end of the exercise, six months later, using two different measurements: cognitive performance tests and magnetic resonance imaging (MRI) to measure variations in the volume of gray matter. This enabled them to observe brain activity and any changes in three areas:

    • the dorsolateral prefrontal cortex that controls planning, decision-making and inhibition;
    • the cerebellum that plays a major role in motor control and balance; and
    • the hippocampus, the centre of spatial and episodic memory.

    According to the MRI test results, only the participants in the video-game cohort saw increases in gray matter volume in the hippocampus and cerebellum. Their short-term memory also improved.

    The tests also revealed gray matter increases in the dorsolateral prefrontal cortex and cerebellum of the participants who took piano lessons, whereas some degree of atrophy was noted in all three areas of the brain among those in the passive control group.

    What mechanism triggers increases in gray matter, especially in the hippocampus, after playing video games? “3-D video games engage the hippocampus into creating a cognitive map, or a mental representation, of the virtual environment that the brain is exploring.,” said West. “Several studies suggest stimulation of the hippocampus increases both functional activity and gray matter within this region.”

    Conversely, when the brain is not learning new things, gray matter atrophies as people age. “The good news is that we can reverse those effects and increase volume by learning something new, and games like Super Mario 64, which activate the hippocampus, seem to hold some potential in that respect,” said West. Added Belleville: “These findings can also be used to drive future research on Alzheimer’s, since there is a link between the volume of the hippocampus and the risk of developing the disease.”

    “It remains to be seen,” concluded West, “whether it is specifically brain activity associated with spatial memory that affects plasticity, or whether it’s simply a matter of learning something new.”


  6. Study suggests genes behind higher education linked to lower risk of Alzheimer’s

    by Ashley

    From the Karolinska Institutet press release:

    Using genetic information, researchers at Karolinska Institutet in Sweden provide new evidence that higher educational attainment is strongly associated with a lower risk of Alzheimer’s disease.

    The causes of Alzheimer’s disease are largely unknown and treatment trials have been disappointing. This has led to increasing interest in the potential for reducing the disease by targeting modifiable risk factors. Many studies have found that education and vascular risk factors are associated with the risk of Alzheimer’s disease, but whether these factors actually cause Alzheimer’s has been difficult to disentangle.

    Mendelian randomisation is a method that uses genetic information to make causal inferences between potential risk factors and disease. If a gene with a specific impact on the risk factor is also associated with the disease, then this indicates that the risk factor is a cause of the disease.

    Susanna C. Larsson, associate professor at the Institute of Environmental Medicine at Karolinska Institutet, and colleagues in Cambridge and Munich, used the Mendelian randomisation approach to assess whether education and different lifestyle and vascular risk factors are associated with Alzheimer’s disease. The analysis included more than 900 genetic variants previously shown to be associated with the risk factors. Comparisons of these genetic variants among 17,000 patients with Alzheimer’s disease and 37,000 healthy controls revealed a strong association for genetic variants that predict education.

    “Our results provide the strongest evidence so far that higher educational attainment is associated with a lower risk of Alzheimer’s disease. Therefore, improving education may substantially decrease the number of people developing this devastating disease,” says Susanna C. Larsson.

    According to the researchers, one possible explanation for this link is ‘cognitive reserve‘, which refers to the ability to recruit and use alternative brain networks or structures not normally used in order to compensate for brain ageing.

    “Evidence suggests that education helps improve brain networks and thus could increase this reserve,” says Susanna C. Larsson.

    The study was financed by the European Union’s Horizon 2020 research and innovation programme and the Swedish Brain Foundation.


  7. Study identifies gene variant that protects against Alzheimer’s disease

    December 11, 2017 by Ashley

    From the Brigham Young University press release:

    Research published Wednesday in Genome Medicine details a novel and promising approach in the effort to treat Alzheimer’s disease.

    Brigham Young University professors Perry Ridge and John Kauwe led the discovery of a rare genetic variant that provides a protective effect for high-risk individuals — elderly people who carry known genetic risk factors for Alzheimer’s — who never acquired the disease.

    In other words, there’s a specific reason why people who should get Alzheimer’s remain healthy. Study authors believe this genetic function could be targeted with drugs to help reduce the risk of people getting the disease.

    “Instead of identifying genetic variants that are causing disease, we wanted to identify genetic variants that are protecting people from developing disease,” said Ridge, assistant professor of biology at BYU. “And we were able to identify a promising genetic variant.”

    That former approach to Alzheimer’s disease has been generally effective in producing a list of genes that might impact risk for the disease, but it leaves researchers without sufficient data on what to do next. In this new approach, Ridge and Kauwe develop the biological mechanism by which a genetic variant actually impacts Alzheimer’s disease.

    Using data from the Utah Population Database — a 20-million-record database of the LDS Church’s genealogical records combined with historical medical records from Utah — Ridge and Kauwe first identified families that had a large number of resilient individuals: those who carried the main genetic risk factor for Alzheimer’s (E4 Allele) but remained healthy into advanced age.

    Using whole genome sequencing and a linkage analysis methodology, they then looked for the DNA that those resilient individuals shared with each other that they didn’t share with loved ones who died of Alzheimer’s. They discovered the resilient subjects shared a variant in the RAB10 gene while those who got the disease did not share the genetic variant.

    Once the researchers identified the potentially protective gene variant, they over expressed it in cells and under expressed it in cells to see the impact on Alzheimer’s disease related proteins. They learned that when this gene is reduced in your body, it has the potential to reduce your risk for Alzheimer’s.

    “There are currently no meaningful interventions for Alzheimer disease; No prevention, no modifying therapies, no cure,” Kauwe said. “The discoveries we’re reporting in this manuscript provide a new target with a new mechanism that we believe has great potential to impact Alzheimer’s disease in the future.”


  8. Study suggests marriage may help stave off dementia

    December 7, 2017 by Ashley

    From the BMJ press release:

    Marriage may lower the risk of developing dementia, concludes a synthesis of the available evidence published online in the Journal of Neurology Neurosurgery & Psychiatry.

    Lifelong singletons and widowers are at heightened risk of developing the disease, the findings indicate, although single status may no longer be quite the health hazard it once seemed to be, the researchers acknowledge.

    They base their findings on data from 15 relevant studies published up to the end of 2016. These looked at the potential role of marital status on dementia risk, and involved more than 800,000 participants from Europe, North and South America, and Asia.

    Married people accounted for between 28 and 80 per cent of people in the included studies; the widowed made up between around 8 and 48 per cent; the divorced between 0 and 16 per cent; and lifelong singletons between 0 and 32.5 per cent.

    Pooled analysis of the data showed that compared with those who were married, lifelong singletons were 42 per cent more likely to develop dementia, after taking account of age and sex.

    Part of this risk might be explained by poorer physical health among lifelong single people, suggest the researchers.

    However, the most recent studies, which included people born after 1927, indicated a risk of 24 per cent, which suggests that this may have lessened over time, although it is not clear why, say the researchers.

    The widowed were 20 per cent more likely to develop dementia than married people, although the strength of this association was somewhat weakened when educational attainment was factored in.

    But bereavement is likely to boost stress levels, which have been associated with impaired nerve signalling and cognitive abilities, the researchers note.

    No such associations were found for those who had divorced their partners, although this may partly be down to the smaller numbers of people of this status included in the studies, the researchers point out.

    But the lower risk among married people persisted even after further more detailed analysis, which, the researchers suggest, reflects “the robustness of the findings.”

    These findings are based on observational studies so no firm conclusions about cause and effect can be drawn, and the researchers point to several caveats, including the design of some of the included studies, and the lack of information on the duration of widowhood or divorce.

    Nevertheless, they proffer several explanations for the associations they found. Marriage may help both partners to have healthier lifestyles, including exercising more, eating a healthy diet, and smoking and drinking less, all of which have been associated with lower risk of dementia.

    Couples may also have more opportunities for social engagement than single people — a factor that has been linked to better health and lower dementia risk, they suggest.

    In a linked editorial, Christopher Chen and Vincent Mok, of, respectively, the National University of Singapore and the Chinese University of Hong Kong, suggest that should marital status be added to the list of modifiable risk factors for dementia, “the challenge remains as to how these observations can be translated into effective means of dementia prevention.”

    The discovery of potentially modifiable risk factors doesn’t mean that dementia can easily be prevented, they emphasise.

    “Therefore, ways of destigmatising dementia and producing dementia-friendly communities more accepting and embracing of the kinds of disruptions that dementia can produce should progress alongside biomedical and public health programmes,” they conclude.


  9. Imaging technique shows progress Alzheimer’s disease

    December 4, 2017 by Ashley

    From the University of Twente press release:

    Using ‘Raman’ optical technology, scientists of the University of Twente in The Netherlands, can now produce images of brain tissue that is affected by Alzheimer’s disease. The images include the surrounding areas, already showing changes.

    Alzheimer’s disease is associated with areas of high protein concentration in brain tissue: plaques and tangles. Raman imaging is now used to get sharp images of these affected areas. It is an attractive technique, because it shows more than the specific proteins involved. The presence of water and lipids, influenced by protein presence, can also be detected. Using this technique, the researchers have studied brain tissue of four brain donors, three of them with Alzheimer’s disease.

    Transition

    The affected area can, in this way, be shown in a sharp and clear way. After image processing, even an area appears that is in transition between healthy and affected tissue: this may give an indication how the disease is spreading in the brain. Even in the brain tissue of the healthy person, a small area is detected with protein activity. This can be a first sign of a neurodegenerative disease.

    Raman microscopy uses a laser beam for the detection of chemical substances. The energy of the reflected and scattered light gives an indication of the substances present in a sample. In each of the four brain samples, 4096 spectra were examined in this way. A major advantage of Raman is that the chemicals don’t need a pretreatment, it is ‘label free’. In chemical analysis, Raman has proven to be a powerful technique.

    Cell level and smaller

    In this case, Raman was used to examine brain tissue outside the body, but it could even be used ‘in vivo’ for detecting specific areas during surgery. Compared to MRI, PET and CT imaging, Raman is able to detect areas, smaller than cells, with very high precision. In this way, it can be a very valuable extra technique. The Raman images now show protein activity at neural cell level, but the sensitivity is high enough for detecting areas that are even smaller — as is the case with the brain sample of the healthy person.

    Cees Otto, of the Medical Cell Biophysics group of UT, published his work in Scientific Reports, together with colleagues from Leiden University and from Spain and Austria.


  10. Study suggests Alzheimer’s Tau protein forms toxic complexes with cell membranes

    December 2, 2017 by Ashley

    From the École polytechnique fédérale de Lausanne press release:

    The brains of patients with Alzheimer’s disease contain characteristic tangles inside neurons. These tangles are formed when a protein called Tau aggregates into twisted fibrils. As a result, the neurons’ transport systems disintegrate, essential nutrients can’t move through, and the cells begin to die, affecting the brain’s functions and giving rise to the disease’s symptoms.

    Given its role in the pathology of Alzheimer’s disease, Tau protein has been extensively investigated. With several clinical trials of amyloid-targeting therapies failing recently, Tau has become one of the most actively pursued therapeutic targets for Alzheimer’s disease. However, questions still remain about how Tau spreads in the brain and kills neurons. The cell membrane has been shown to play a role in regulating Tau’s aggregation properties and physiological functions, but we still do not understand how the interplay between Tau and lipid membranes can lead to the loss of neurons seen in Alzheimer’s disease.

    Now, the lab of Hilal Lashuel at EPFL, in collaboration with the lab of Thomas Walz at the Rockefeller University, found that individual Tau proteins interact with and disrupt the cell membrane of neurons. This disruption gives rise to highly stable complexes made up of several Tau proteins as well as fat molecules (phospholipids) from the membrane.

    Subsequent studies showed that the protein/phospholipid complexes are more readily taken up by neurons compared to the fibril form of the protein, and induce toxicity in primary neurons of the hippocampus in vitro. The hippocampus is where memory is processed, and loss of hippocampal neurons is a classic symptom of Alzheimer’s disease. The complexes were detectable with an antibody (MC-1) that is used as a standard for detecting pathological conformations of Tau, meaning that they share some features of the pathological form of the protein.

    “Our goal was to identify the sequence and structural factors that drive Tau interaction with membranes and the formation of these complexes so that we can develop strategies to interfere with their formation and block their toxicity,” says Nadine Ait Bouziad, the PhD student who led the study.

    In collaboration with Professor David Eliezer at Weill Cornell School of Medical Sciences in New York, the researchers used Nuclear Magnetic Resonance (NMR) to gain insight into the structure of Tau in the core of the complexes. This revealed that the cores are made up of two small peptides, each only six amino acids long. These peptides are called PHF6* and PHF6, and they play important roles in driving Tau aggregation and assembly into fibrils. Their presence connects the protein/phospholipid complexes with the development of Alzheimer’s disease.

    Building on their findings, the researchers were able to produce mutant Tau protein. The introduced mutations disrupted Tau’s ability to interact with cell membranes, but did so without interfering with its ability to form fibrils. The idea behind this is that such mutants can be used to uncouple these two processes, which would allow researchers to investigate the effect that these membrane interactions have on the function, aggregation and toxicity of Tau in primary neuron cultures. This would be a first step in gaining a clearer picture of how Tau tangles begin to form, which would be critical if we are to develop efficient therapies to counteract their toxicity.

    “Our findings point toward a novel form of Tau protein/phospholipid complexes that might be part of a membrane-dependent mechanism that regulates Tau structure, oligomerization, toxicity, and possibly its normal and aberrant trafficking between and within neurons,” says Hilal Lashuel. “By developing tools that allow us to detect, disrupt and/or target these complexes, we hope to identify novel strategies to inhibit Tau aggregation, toxicity, and pathology spreading in the Alzheimer’s brain.”