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Results from the phase 2 TRAILBLAZER-ALZ were presented at the 15th International Conference on Alzheimer & Parkinson DiseasesTM 2021.

 The new data expanded on earlier top-line data for donanemab, and was also published in the 

 Not only did donanemab meet its primary endpoint, but it also showed significant slowing of decline on the integrated Alzheimer Disease Rating Scale (iADRS) in participants with early Alzheimer disease when compared to placebo.

“We are confident in the results of the TRAILBLAZER-ALZ study,” Daniel Skovronsky, MD, PhD, Eli Lilly and Company’s chief scientific officer and president of Lilly Research Laboratories, said to the press. “This is the first late-stage study in Alzheimer disease to meet its primary endpoint at the primary analysis. Donanemab has the potential to become a very important treatment for Alzheimer disease.”

Donanemab, a monoclonal antibody, was designed to target a particular form of post-translationally modified Aß, N-terminal pyroglutamate, and completely clear amyloid plaques.

Secondary analyses showed donanemab consistently slowed cognitive and functional decline, with ranges between 20% to 40% in all secondary endpoints. Analyses also showed donanemab slowed the accumulation of tau across important brain regions in participants with Alzheimer disease. 

“We were pleased to see not only slowing of cognitive and functional decline, but also very substantial clearance of amyloid plaques and slowing of spread of tau pathology,” Skovronsky further noted. “The constellation of clinical and biomarker results indicates the potential for long-term disease modification. We are grateful to the patients, caregivers, and investigators who participated in this landmark study.”

Treatment with donanemab slowed decline by 32% when compared to placebo, measured by the iADRS, at 76 weeks compared to baseline. This was statistically significant. Noticeable difference in decline was observed as early as 36 weeks after initiation of treatment. About 40% of participants achieved amyloid negativity after treatment with donanemab as early as 6 months into treatment, and 68% achieved negativity by 18 months into treatment.

“Tau has become increasingly validated as a predictive biomarker for Alzheimer's disease progression, as shown again in this trial,” said Liana G. Apostolova, MD, MSc, FAAN, Indiana University (IU) Distinguished Professor and Barbara and Peer Baekgaard Professor in Alzheimer Disease Research at IU School of Medicine. “A key insight of the results from the TRAILBLAZER-ALZ study is that donanemab not only significantly reduced the amount of amyloid deposition in these patients but also slowed the clinical progression of the disease suggesting that this could be a disease-modifying therapy. We believe these amyloid and tau imaging data lay the foundation for precision medicine-based Alzheimer disease treatments.”

Stephen P. Salloway, MS, MD, Director of the Memory and Aging Program and the Department of Neurology at Butler Hospital, Martin M. Zucker professor of Psychiatry and Human Behavior at Warren Alpert Medical School of Brown University, added: “As a clinician and researcher, I’m particularly encouraged by the significant plaque lowering and the slowing of clinical decline with donanemab. The donanemab results are a significant and encouraging milestone for people impacted by Alzheimer disease and we are eager to continue on in this fight.”

1. Eli Lilly and Company. Lilly's donanemab slowed Alzheimer’s disease progression in Phase 2 trial: full data presented at AD/PD™ 2021 and published in NEJM. 

https://www.prnewswire.com/news-releases/lillys-donanemab-slowed-alzheimers-disease-progression-in-phase-2-trial-full-data-presented-at-adpd-2021-and-published-in-nejm-301246745.html

2. Mintun MA, Lo AC, Evans CD, et al. Donanemab in early Alzheimer’s disease. 

https://www.nejm.org/doi/full/10.1056/NEJMoa2100708

This monoclonal antibody showed significant slowing of decline in patients with Alzheimer disease. 

New Data for Alzheimer Agent Presented at International Conference

The medical science and research company Clarivate has named aducanumab, a potential Alzheimer disease (AD) treatment, as one of its top 5 “Drugs to Watch 2021.”

 Clarivate, which has published the “Drugs to Watch” list 

, included aducanumab on the list because it has a new mechanism of action and would be the first novel therapeutic for AD in more than 15 years. The company selects drugs in phase 2 or 3 trials that have the potential to bring in $1 billion in sales 

. Aducanumab is in phase 3 trials, and the US Food and Drug Administration (FDA) has promised to render its verdict in June.

, expects it will be a game changer. Lavretsky, professor in-residence in the Department of Psychiatry at the University of California, Los Angeles, told 

, “It will revolutionize Alzheimer disease treatment and care, and will have a profound impact on the lives of millions of family caregivers, who will be relieved from caring for their relatives, or the time of caregiving will be shortened, improving lives of millions of people around the world, and reducing the cost of the disease to the society.”

Aducanumab would be the first approved drug in the last 15 years that could slow down the cognitive decline associated with AD. 

, for cases across the spectrum from mild to severe, are 

The drug might address a root cause of AD. It builds on the amyloid cascade hypothesis, in which “production and accumulation of excessive amyloid-β (Aβ) may be the main cause in the onset and progression of Alzheimer's disease.”

 If so, removing or lowering of Aβ in patients with presymptomatic and early AD could be an effective therapy, and even used as a preventive, subunit vaccine.

, noted, “this drug will be the first antiamyloid therapy and disease modifying therapy for Alzheimer disease.” Tampi is professor and chairman of the Department of Psychiatry & Behavioral Sciences at the Cleveland Clinic. Lavretsky described aducanumab as a “breakthrough treatment with a novel mechanism as recombinant chimeric human IgG1 mAb targeting beta-amyloid.”

Excitement is especially strong for the drug since innovation in therapies for AD has been frustratingly slow. The problem, Tampi explained, is that AD is caused by neurological degeneration, and “it is very difficult to develop different therapies to reverse these neurobiological changes in the brain.”

Finding effective treatments has also been difficult due to “uncertainty about the underlying mechanisms of the disease, the reliance on postmortem diagnosis, and the lack of reliable biomarkers for disease early diagnosis and progression, despite almost 120-year history of research,” Lavretsky added. “Many potential therapies failed to document efficacy and did not achieve the FDA approvals.”

Sure enough, despite its promise, aducanumab has had its own set of struggles. Last November brought disappointment, when the FDA published a negative review of aducanumab, citing insufficient evidence of clinical efficacy.

The news was especially disappointing, given aducanumab’s success in previous trials. In 2015, aducanumab underwent two phase 3 efficacy trials.

 The 221AD301 ENGAGE study enrolled 1350 participants with mild cognitive impairment due to AD. It compared monthly infusions of 1 or 3 doses of aducanumab with placebo over an 18-month period, and their effects on cognitive decline. In 2017 and 2018, data from the trials showed that the treatment was slowing cognitive decline. Consequently, aducanumab became the first such DMT for AD to demonstrate clinical efficacy in a phase 3 trial.

However, in March 2019 Biogen and Eisai announced termination of ongoing aducanumab trials, due to missing primary endpoints.

 Despite the termination, further analysis of the data suggested that a subgroup of participants experienced slower cognitive decline.

Trials resumed on January 27, 2020, when Biogen announced a phase 3b study of 2400 participants who had previously used aducanumab.

 Participants were scheduled to receive monthly injections over the next 2 years. Based on this trial, Biogen requested priority review from the FDA for licensing. The FDA turned down the application in November 2020, citing the weakness of efficacy data.

After aducanumab’s developers, Biogen Inc and Eisai Co Ltd, submitted additional data, the FDA extended its decision date to June 7, 2021.

If approved, aducanumab would meet an enormous need.

“It will offer a new hope to patients and their families and therapeutic optimism to geriatric clinicians and researchers,” said Lavretsky.

https://clarivate.com/drugs-to-watch/drugs-to-watch-listing/aducanumab/

2. Yu YZ, Xu Q. Prophylactic immunotherapy of Alzheimer's disease using recombinant amyloid-β B-cell epitope chimeric protein as subunit vaccine. 

3. Talan J. FDA Panel Votes ‘No’ to Approving Audcanumab for Alzheimer’s, Citing Inconsistent Data. 

. December 3, 2020. Accessed March 9, 2021. 

https://journals.lww.com/neurotodayonline/Fulltext/2020/12030/FDA_Panel_Votes__No__to_Approving_Aducanumab_for.1.aspx

4. Aducanumab. Therapeutics. Alzforum: networking for a cure. Accessed March 9, 2021. 

https://www.alzforum.org/therapeutics/aducanumab

5. Biogen/Eisai Halt Phase 3 Aducanumab Trials. Alzforum: networking for a cure. March 21, 2019. Accessed March 9, 2021. 

https://www.alzforum.org/news/research-news/biogeneisai-halt-phase-3-aducanumab-trials

6. Biogen and Eisai Announce FDA’s 3-Month Extension of Review Period for the Biologics License Application for Aducanumab. News release. GlobeNewswire. January 29, 2021. Accessed March 9, 2021. 

https://www.globenewswire.com/news-release/2021/01/29/2166560/0/en/Biogen-and-Eisai-Announce-FDA-s-3-Month-Extension-of-Review-Period-for-the-Biologics-License-Application-for-Aducanumab.html

Aducanumab is named 1 of the 5 “Drugs to Watch” for 2021.

Is the First Disease-Modifying Therapy for Alzheimer Disease on the Horizon?

The prognosis for an Alzheimer disease (AD) vaccine remains uncertain, but there is potential for this new treatment. Biopharmaceutical company AC Immune announced positive interim results from its phase 1b/2a clinical trial studying its Alzheimer disease vaccine, ACI-35.030.

“These remarkable data show that ACI-35.030 is capable of generating unprecedented antibody responses against pTau in an elderly population, with very high antigen-specific titers. Importantly, it generated a much stronger antibody response compared to direct injection of exogenous antibodies,” CEO of AC Immune Andrea Pfeifer, PhD, said. “As pathological pTau is present as a precursor many years before Tau accumulation in the brain is detectable via brain imaging, such results highlight the significant promise of ACI-35.030 as an early intervention for AD, especially when combined with cutting-edge pTau diagnostics that would enable identification of people at risk of developing Tau-driven disease.”

ACI-35.030 is a potent liposomal anti-pTau active investigational vaccine designed to elicit antibodies against phosphorylated pathological Tau protein.

The study, while relatively small with only 32 participants and 2 dose cohorts,

 discovered a potent antigen-specific antibody response against pTau in older patients with early AD. The vaccine achieved antibody levels several degrees of magnitude higher than prevaccination levels, and no clinically relevant adverse events were observed.

The interim data showed that anti-Tau IgG response preferentially targets phosphorylated Tau in all participants, very high anti-pTau IgG titers were observed following injection, and a demonstrated anti-pTau IgG response in all participants after the 1st injection.

But despite these encouraging signs, the data release had little in terms of concrete data, with no number attached to the supposed increased antibody levels or any median increase across the study. While this has left some investors skeptical,

 AC Immune and their strategic partner Janssen Pharmaceuticals plan to advance the development of ACI-35.030 for the treatment of AD.

“We look forward to continuing to advance ACI-35.030 in our collaboration with Janssen Pharmaceuticals, Inc, as we aim to bring this potentially breakthrough vaccine to patients,” Pfeifer said further.

1. AC Immune. AC Immune’s Alzheimer’s vaccine generates potent anti-pTau antibody response in a phase 1b/2a study. News release. February 11, 2021. 

https://ir.acimmune.com/news-releases/news-release-details/ac-immunes-alzheimers-vaccine-generates-potent-anti-ptau

2. Mast J. AC Immune has ‘remarkable’ Alzheimer’s vaccine data. Just don’t ask to see them. 

https://endpts.com/ac-immune-has-remarkable-alzheimers-vaccine-data-just-dont-ask-to-see-them/

A study on a new Alzheimer disease vaccine lacks concrete numbers. 

Alzheimer Disease Vaccine: Less Talk, More Numbers

Cognitive impairment is not always associated with dementia. For this reason, a full comprehensive history is an integral component of any assessment. Take the quiz to learn more.

Mini Quiz: Evaluating Dementia

BioXcel Therapeutics recently announced that its orally dissolving, thin-film formulation of dexmedetomidine, BXCL501, met the primary and secondary endpoints of the TRANQUILITY trial at the 60 mcg dose level.

“We are very encouraged by the promising topline results from the TRANQUILITY study, which was designed to identify a recommended dose of BXCL501 for a potential pivotal study in dementia patients suffering from agitation. Following decades of research, there are still no effective treatments that directly target agitation commonly seen with dementia patients, and we are thrilled by the potential of being the first to develop a therapy designed to address this significant patient and caregiver need,” Vimal Mehta, Chief Executive Officer of BioXcel, said to the press. “Based on the results observed, we believe BXCL501 has broad potential in treating the full spectrum of agitation in patients with dementia. We look forward to advancing BXCL501 into a late-stage study this year following dialogue with the FDA.”

BXCL501 is a selective alpha-2a receptor agonist for the treatment of agitation and opioid withdrawal symptoms. BioXcel believes that BXCL501 directly targets an agitation mechanism and has observed anti-agitation results in a number of clinical studies across several neuropsychiatric disorders.

The US Food and Drug Administration (FDA) granted BXCL501 Fast Track Designation for the acute treatment of agitation in patients with schizophrenia, bipolar disorders, and dementia. Two different phase 3 trials (SERENITY I and II) studied BXCL501 for the acute treatment of agitation associated with schizophrenia and bipolar disorders.

The TRANQUILITY study consisted of 54 participants in assisted living facilities with agitation related to dementia, 87% of whom had Alzheimer disease. Participants received BXCL501 at either 30 mcg, 60 mcg, 90 mcg, or a placebo. Participants reported no severe or serious adverse events, and the primary safety and tolerability endpoints were met. Adverse events in the trial included hypotension, orthostatic hypotension, and dizziness, with the most common adverse event being mild or moderate somnolence.

BioXcel also shared plans for a phase 2 trial studying hospitalized patients who have agitation symptoms associated with delirium, intended to begin within the next several months.

1. BioXcel Therapeutics. BioXcel Therapeutics announces BXCL501 met the primary and all secondary endpoints in the TRANQUILITY phase 1b/2 study for the acute treatment of agitation in dementia, including Alzheimer disease. News release. 

https://www.globenewswire.com/news-release/2021/01/05/2153316/0/en/BioXcel-Therapeutics-Announces-BXCL501-Met-the-Primary-and-All-Secondary-Endpoints-in-the-TRANQUILITY-Phase-1b-2-Study-for-the-Acute-Treatment-of-Agitation-in-Dementia-including-Al.html

A new formulation of dexmedetomidine meets primary and secondary endpoints in recently completed study. 

Medication for Agitation in Dementia and Alzheimer Disease Patients Moves Forward

In the United States, there are currently no Federal Drug Administration (FDA) approved medications for the treatment of psychosis in Alzheimer disease (AD). This is a problem because approximately 25% to 50% of individuals with AD develop psychosis during their illness, and 

But a recent trial found that pimavanserin reduced psychosis symptoms in patients with AD. According to Rajesh Tampi, MD, MS, DFAPA, 

 neuropsychiatry section editor, this research could be ground-breaking because “pimavanserin will be the first drug, if approved, for this indication in the US with an indication for psychosis in AD.”

Pimavanserin could improve patient outcomes significantly. Existing antipsychotic drugs may be effective for treating delusions and hallucinations, but antipsychotics are also associated with increased risk for death, cerebrovascular adverse events, sedation, falls, and pneumonia. Given these concerns, effective and safe pharmacological treatment of psychosis in AD remains a pressing need.

A literature review of clinical studies on pimavanserin as a treatment for psychosis concluded that “pimavanserin may be a pharmacologic consideration for the treatment of psychosis in AD.”

 In 2 publications, pimavanserin improved psychotic symptoms in individuals with AD when compared with a placebo after 6 weeks. The authors of the literature review warned that further randomized controlled trials were needed before pimavanserin could be considered a standard treatment.

 to the FDA, asking it to approve pimavanserin for dementia-related psychosis.

 A serotonergic agent and selective serotonin (5-HT) 2A receptor inverse agonist, pimavanserin may be able to treat hallucinations and delusions.

Acadia’s study is a Phrase 3 trial that began in 2019. It included 117 study locations, scattered across the US, Europe, and Chile, and enrolled 392 participants with dementia who had suffered from symptoms of psychosis for at least the last 2 months.

 Following a 12-week open-label period, participants who responded were broken into 2 groups for the following 26 weeks, in which 1 received a placebo and the other pimavanserin. The study then followed the patients until they had a relapse, defined by hospitalization as a result of dementia-related psychosis, deterioration of dementia symptoms, withdrawal from the study due to lack of efficacy, or use of another antipsychotic medication. 

Acadia reported that pimavanserin significantly reduced the risk of a relapse. Those on the placebo were 2.8 times more likely to relapse during the study period. Given promising results, they filed a supplemental New Drug Application (sNDA) with the FDA.

Pimavanserin is already FDA approved for the treatment of hallucinations and delusions in individuals with Parkinson disease psychosis (PDS), but the same symptoms have no standard drug treatment for individuals with dementia-related psychosis. The FDA will likely not render a verdict before April 2021, but clinicians may want to keep this research in mind, as it could be an indication for using pimavanserin in the near future.

1. Srinivasan S, Tampi RR, Balaram K, Kapoor A. Pimavanserin for the treatment of psychosis in Alzheimer's disease: A literature review. 

2. Pimavanserin – dementia-related psychosis. News release. Acadia Pharmaceuticals, Inc. Accessed November 9, 2020. https://www.acadia-pharm.com/pipeline/pimavanserin-drp/

3. Pimavanserin. Alzforum: networking for a cure. Updated July 24, 2020. Accessed November 9, 2020. 

https://www.alzforum.org/therapeutics/pimavanserin

A new treatment for hallucinations and delusions in individuals with Alzheimer disease may be on the horizon. 

Hope for Dementia-Related Psychosis 

A pair of trials related to Alzheimer disease recently released big news: NovoNordisk decided to move its recently launched type 2 diabetes drug semaglutide into a phase 3 study, and AB Science SA shared the results from a phase 2B/3 study evaluating masitinib in Alzheimer disease.

NovoNordisk’s type 2 diabetes (T2D) drug, semaglutide, will be the first-to-market oral GLP-1RA in T2D. However, after the large number of failures in Alzheimer disease trials in 2019, several key opinion leaders believe NovoNordisk will face a tough battle when entering into Alzheimer disease market.

Valentina Gburcik, PhD, Senior Director of Cardiovascular and Metabolic Diseases, Gender Health and Digital at GlobalData, had this to say on semaglutide: “Due to the growing unmet needs in the Alzheimer’s space, which has not seen any major medical breakthroughs over the past decade, and the increasing evidence of a potential therapeutic role for GLP-1, oral semaglutide may be able to secure its position in a yet another lucrative market if found to be efficacious in challenging Alzheimer’s clinical trials. However, the drug may face fierce competition from a number of novel therapies entering the Alzheimer’s market over the next several years.”

On the topic of masitinib, AB Science SA presented data confirming that masitnib’s mode of action has a potential synergistic effect and 4 targets. The 4 targets of masitinib in Alzheimer disease are:

1. Modulation of microglia: masitinib modulates microglia activity through inhibition of the CSFR-1 kinase and is involved in the neuroinflammatory processes commonly associated with Alzheimer disease.

2. Protecting synapses: Alzheimer disease alters synapses, and masitinib has been shown to promote recovery of synaptic markers in mouse models.

3. Inhibiting the tau protein: masitinib inhibits the FYN kinase, a kinase that mediates tau phosphorylation, and also prevents the accumulation of amyloid fibrils in the hippocampus, as shown in mouse models.

4. Control of mast cell activity: masitinib blocks mast cells activity through inhibition of the c-Kit, LYN, and FYN kinases. Mouse models showed that mice depleted of mast cells do not develop symptoms of Alzheimer disease.

In a transgenic mouse model, masitinib was able to restore cognitive impairment and restore ability to perform navigation strategy in the Morris Water Maze experiment. It could also exert a neuroprotective effect against synaptic loss.

“Study AB09004 was a well-designed phase 2b/3 as it compared masitinib on top of standard of care treatment versus the standard of care. These data are very encouraging and may provide new hope for patients with Alzheimer’s disease,” Bruno Dubois, MD, PhD, professor of neurology at the Neurological Institute of the Salpétrière University Hospital at Paris and coordinating investigator of the study, said to the press.

These announcements point to big changes on the horizon for the treatment of Alzheimer disease. Further discoveries and products will hopefully bring clinicians and researchers a step closer to a cure. 

1. GlobalData. NovoNordisk’s Rybelsus a game changer in T2D but may face a tough road ahead as it strides into Alzheimer’s space. News release. December 18, 2020. 

https://www.globaldata.com/novonordisks-rybelsus-game-changer-t2d-may-face-tough-road-ahead-strides-alzheimers-space/

2. AB Science. AB Science communicates the results from phase 2B/3 study evaluating masitinib in Alzheimer’s disease. News release. 

https://www.globenewswire.com/news-release/2020/12/18/2147549/0/en/AB-Science-communicates-the-results-from-phase-2B-3-study-evaluating-masitinib-in-Alzheimer-s-disease.html

New developments in Alzheimer disease treatment and research. 

Breakthroughs in Alzheimer Disease

The Lumipulse® G β-Amyloid Ratio in vitro diagnostic test was filed for 510(k) premarket clearance with the US Food and Drug Administration (FDA), Fujirebio Diagnostics, Inc, announced today. In February 2019, the test was granted Breakthrough Device Designation. It is expected to be one of the first US in vitro diagnostic tests for the assessment of Alzheimer disease.

“The lack of effective and accessible clinical tools for patients who could be on the pathway to develop Alzheimer disease contributes to its late diagnosis and inadequate treatment,” Monte Wiltse, President and CEO at Fujirebio Diagnostics, said to the press. “We designed our Lumipulse® G β-Amyloid Ratio test to help physicians triage their patient much sooner when effective interventions are more feasible using these well- researched β-amyloid biomarkers. Accurate and earlier intervention will also facilitate the development of new drug therapies, which are urgently needed as the prevalence of Alzheimer disease increases with a rapidly aging population globally.”

Alzheimer disease is diagnosed in more than 5 million Americans, with few treatments available until their disease is further advanced. Current tools, like amyloid PET imaging, can be expensive, time consuming, and hard to access.

The Lumipulse G β-Amyloid Ratio is reported to merge the concentrations of Lumipulse G β-Amyloid 1-42 and Lumipulse G β-Amyloid 1-40 found in human cerebral spinal fluid (CSF). It is intended for use in patients aged 50 years and over who present with cognitive impairment and are being evaluated for Alzheimer disease. It is also not intended for sole use, but rather to be used in conjunction with other diagnostic modalities. Fujirebio’s fully automated LUMIPULSE® G1200 instrument system analyzes the test.

It is the hope of researchers that better diagnostics will spur the developments of further treatments options.

1. Fujirebio Diagnostics. Fujirebio Diagnostics Files 510(k) With FDA for Lumipulse® G β-Amyloid Ratio (1-42/1-40) In Vitro Diagnostic Test. News release. December 2, 2020. 

https://www.fujirebio.com/en-us/news-events/fujirebio-diagnostics-files-510k-with-fda-for-lumipulser-g-bamyloid-ratio-142140-in

The Lumipulse® G β-Amyloid Ratio in vitro diagnostic test was filed for 510(k) premarket clearance. 

One of the First US In Vitro Diagnostic Tests for Assessment of Alzheimer Disease

 led by The Jackson Laboratory and University of Maine has discovered that the gene Dlgap2 is associated with Alzheimer disease, dementia, and cognitive decline. Researchers found post-mortem human brain tissues of individuals experiencing “poorer cognitive health” and “faster cognitive decline” had low levels of Dlgap2.

“The reason why this is so important is because a lot of research around cognitive aging and Alzheimer’s has been hyper-focused on well-known risk genes like APOE and brain pathologies,” Catherine Kaczorowski, associate professor and Evnin family chair in Alzheimer disease research at The Jackson Laboratory (JAX), and adjunct professor with the University of Maine Graduate School of Biomedical Science and Engineering (GSBSE), said to the press. “We wanted to give ourselves the option of looking at new things people keep ignoring because they've never heard about a gene before.”

Located in the synapses of neurons, Dlgap2 anchors critical receptors for signals between learning and memory neurons. The research team examined the memory and brain tissue from a large group of genetically diverse mice, relying on diversity outbred mice. The population came from 8 parents created by JAX, as they thought a diversified group would better reflect genetic diversity in humans. About 437 mice, each either 6, 12, or 18 months old were used.

“It’s great because you can harness the best parts of a mouse study and human society,” Andrew Ouellette, a PhD student at JAX and a GSBSE NIH T32 predoctoral awardee, said to the press. “Historically, research has been done with inbred mice with similar genetic makeups; same, similar genetic models. But clinically, humans don't work like that because they're not genetically identical.”

Quantitative trait loci mapping was performed on the mouse population. Study of entire genome sequences allowed for identification of the genes responsible for varying cognitive function and where they occurred. Researchers pinpointed the connection between Dlgap2 and memory decline in mice, and were then able to evaluate its significance to humans.

They found Dlgap2 is associated with the degree of memory loss in mice and risk for Alzheimer dementia in humans. Further research will be needed to determine how the gene influences dementia and brain functioning.

1. Ouellette AR, Neuner SM, Dumitrescu L, Hadad N, et al. Cross-species analyses identify Dlgap2 as a regulator of age-related cognitive decline and alzheimer’s dementia. 

2. University of Maine. New connection between Alzheimer's dementia and Dlgap2. News release. 

https://www.sciencedaily.com/releases/2020/11/201123161040.htm

A new study associates a gene that facilitates neuron communication in the nervous system with memory loss. 

Dlgap2: The Gene Associated With Memory Loss

Christopher J. Barnum, PhD, of INmune Bio, Inc discusses XPro1595, developed by INmune Bio, and how it may provide neuroprotective benefits for those at risk of developing Alzheimer disease. 

Rather than focusing on amyloid or tau clearing therapies like many that have come before, this treatment takes a unique approach to tackling neuroinflammation by

 selectively neutralizing soluble tumor necrosis factor (sTNF). This is a 

a “bad” cytokine that is elevated in many chronic neurodegenerative and neuroinflammatory conditions. 

In addition to this video, Dr Barnum recommends watching 

is the Director of Neuroscience at INmune Bio, Inc. Dr Barnum is a neuroimmunologist with broad expertise across neurodegenerative and psychiatric diseases holding multiple positions in academia and industry, including Emory University, FPRT Bio, SonosBio, and most recently Takeda Pharmaceuticals. His focus has been on translating inflammatory therapies into clinical treatments for neurologic diseases using a biomarker-directed approach. Dr Barnum has been working with XPro1595 for more than a decade, first at Emory University with Dr Malú Tansey and subsequently as a consultant for FPRT Bio, Inc and INmune Bio, before joining INmune Bio full time in 2018. Dr Barnum’s research has been supported by NIH, The Michael J Fox Foundation, and the Alzheimer’s Association. He received his PhD in Neuroscience from Binghamton University.

Patients with chronic inflammatory diseases, especially rheumatoid arthritis, are at 800% increased risk for developing Alzheimer disease compared to the general population. A new treatment is in the works to combat this inflammation. 

Alzheimer Disease