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A plea for equitable global access to COVID-19 diagnostics, vaccination and therapy: the NeuroCOVID-19 task Force of the european Academy of neurology…

This article was originally published here

Eur J Neurol. 2021 Jan 18. doi: 10.1111/ene.14741. Online ahead of print.

ABSTRACT

Coronavirus disease 2019 (COVID-19), a multi-organ disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to challenge health and care systems around the globe. The pandemic has disrupted acute neurology services and routine patient care and has impacted the clinical course in patients with chronic neurologic disease. COVID-19 appears to have exposed inequalities of societies and healthcare systems and had disproportionate impact on already vulnerable communities. The next challenge will be to set up initiatives to stop disparities in all aspects related to COVID-19. From the medical perspective, there is a need to consider inequalities in prevention, treatment, and long-term consequences. Some of the issues of direct relevance to neurologists are summarised. With this appraisal, the European Academy of Neurology NeuroCOVID-19 Task Force intends to raise awareness of the potential impact of COVID-19 on inequalities in healthcare and calls for action to prevent disparity at individual, national and supranational level.

PMID:33460486 | DOI:10.1111/ene.14741

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Optic Nerve Data Helps Boost Diagnostic Performance Among Patients With MS – Neurology Advisor

Researchers from the Universitat Autnoma de Barcelona in Spain found that incorporating features of the optic nerve into multiple sclerosis (MS) diagnostic criteria improved diagnostic performance by increasing sensitivity without lowering specificity, according to study results published in Neurology.

Data for this study came from a prospective study of 1238 patients diagnosed with clinically isolated syndrome after a single magnetic resonance imaging (MRI) scan performed between 1995 and 2017. Study investigators retrospectively assessed data of visual evoked potentials through patient medical records. They split patients into risk assessment (n=388) and diagnostic criteria performance (n=151) cohorts to validate whether MS diagnostic criteria improved with the addition of optic nerve information.

At clinically isolated syndrome diagnosis, patients were a mean age of 31.6 (standard deviation [SD], 8.2 years). 68% of patients were women; 63.6% had nonoptic neuritis; 58.8% were positive for oligoclonal bands; 71.2% had an abnormal MRI; 37.8% had abnormal visual evoked potentials; and the median extended disability status scale was 1 (range, 0-5.5).

Among cohort 1, persons with higher levels of diagnostic criteria were at increased risk for a second attack from 1 criterion (hazard ratio [HR] 5.6; 95% CI, 1.9-16.5) to 5 criteria (HR 22.7; 95% CI, 7.9-65.7).

The 2017 dissemination in space (DIS) criteria identified a similar risk for second attack (HR, 4.3; 95% CI, 2.8-6.5) as the modified DIS (modDIS) (HR, 4.8; 95% CI, 3.0-7.5). Stratified by optic nerve involvement, the risk for a second attack was projected to be elevated among patients with optic neuritis using the modDIS (HR, 4.3; 95% CI, 1.9-9.6) compared with 2017 DIS (HR, 3.8; 95% CI, 1.8-8.0).

Among cohort 2, identifying the risk for second attack at 10 years according to the 2017 DIS was less precise (sensitivity, 79.2%; specificity, 52.4%; accuracy, 75.5%; positive predictive value [PPV], 91.1%; negative predictive value [NPV], 28.9%) compared with the modDIS (sensitivity, 82.3%; specificity, 52.4%; accuracy, 78.1%; PPV, 91.4%; NPV, 32.3%).

Similarly, among only the patients with optic neuritis, the 2017 DIS predicted a second attack at 10 years with a poorer overall performance (sensitivity, 69.7%; specificity, 57.1%; accuracy, 67.5%; PPV, 88.5%; NPV, 28.6%) compared with the modDIS criteria (sensitivity, 75.8%; specificity, 57.1%; accuracy, 72.5%; PPV, 89.3%; NPV, 33.3%).

This study may have included some selection bias, as researchers included only patients with complete medical records in the 2 cohorts analyzed here.

According to their findings, the study researchers concluded that the addition of the optic nerve to the current DIS criteria slightly increases the accuracy and sensitivity without lowering the specificity, providing additional evidence that argues in favor of including the optic nerve as a new region in the diagnostic criteria.

Disclosure: Multiple authors declared affiliations with industry. Please refer to the original article for a full list of authors disclosures.

Reference

Vidal-Jordana A, Rovira A, Arrambide G, et al. Optic nerve region in multiple sclerosis diagnosis: the utility of visual evoked potentials. Published online December 16, 2020. Neurology. doi:10.1212/WNL.0000000000011339

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My wife has a degenerative neurological disease. My father-in-law wants to put her in a facility and take over our finances – MarketWatch

Dear Moneyist,

I have been married for 24 years. My wife and I have two 18-year-old children. We have had our marital ups and downs as many do, but manage to get along. My wife was diagnosed with a terminal degenerative neurological condition.

She grows increasingly frail, both physically and cognitively. Although at times it is not easy, myself and our two children, who are home from school due to the pandemic, care for her the best we can. She lives very comfortably in the home we have owned for 20 years.

The Moneyist:I took care of my late mother for 8 years. Am I obliged to tell my sisters she made me co-owner of a substantial bank account?

My wifes family is largely dysfunctional, and her father abandoned her as a young child, never returning in any meaningful way or providing support aside from cards and perfunctory holiday pleasantries. I do not get along with my father-in-law and have largely avoided him.

Upon learning of my wifes condition, my father-in-law now seems obsessed with moving my wife out of our home to some sort of group home/facility. The mere thought of this seems abhorrent and barbaric. My thinking is that he intends to obtain guardianship and access marital assets, mainly our home, which has substantial value and equity.

My greatest wish is to avoid a bitter legal fight in my wifes last years, and provide her with the best care, medical and otherwise.

Devoted Husband

Want to read more?Follow Quentin Fottrell on Twitterand read more of his columns here

Dear Devoted,

Tell your father-in-law that you have heard his opinion, but now you and your children need to take care of your wife at home together as a family, in your own way, and ask him to respect your wishes. If he continues, tell him that you understand that this is an uncertain and concerning time for all of you, but you would like him to trust you and your family to take care of your wife and his daughter. If that doesnt work, you can say, I now need time and space now to take care of things here. I hope you can give me that. You dont have to answer every call and email.

I also advise you to talk to your wife about officially becoming her health-care proxy, so you will be in control of making any life or death decisions concerning her condition. Alternatively, talk to a lawyer about this. Its smart to have a health-care proxy, no matter how old you are or whether or not youre married, according to Care.com. And a health-care proxy also allows you to designate an alternate, so if you and your spouse are in an accident together you still have control over whos making health-care decisions on your behalf.

Similarly, Leanna Hamill, a family attorney in Hingham, Mass., says, If your parents and spouse disagree about your care, this can cause real problems. The best thing to do is execute a health-care proxy appointing the person you choose as your health care agent and then talking to that person and your other family members about your wishes. (Lawyers want to avoid the kind of legal trauma surrounding the life and death of Terry Schiavo.) Regardless, doctors will turn to your wifes next of kin for any vital decisions that need to be made regarding her care. Thats you.

The Moneyist: My son inherited money after his father was killed in an accident. A woman came forward with another legal heir. What now?

But there is no reason to assume the same will happen here. You will feel less anxious about your father-in-laws interference when you speak up. You dont have to be held hostage to other peoples wishes. Lets assume he wants what he believes is best for his daughter. You simply have a different opinion and approach. He cant force you to sell your home or refinance your home to do something you dont want to do. You are probably under more stress than you realize, and his interference may be a proxy for that stress. It is, perhaps, an obvious if not exactly a useful place to put it.

In the meantime, I recommend seeking out counseling and/or support to help you through this difficult time. The Well Spouse Association is a nonprofit organization that has support groups in communities all over the country. Your wifes condition and comfort is, of course, your No. 1 priority. Dont allow other family members, friends or neighbors to distract you from that. You can only do so much. By creating a support network and healthy boundaries with others however well-meaning they may be I have no doubt that your commitment to your wifes care will be enough.

The Moneyist: My mothers husband died. Her savings are dwindling, yet she pays my sisters bills. Should I intervene?

You can email The Moneyist with any financial and ethical questions related to coronavirus at qfottrell@marketwatch.com

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Hello there, MarketWatchers. Check out the Moneyist private Facebook FB, +3.87% group where we look for answers to lifes thorniest money issues. Readers write in to me with all sorts of dilemmas. Post your questions, tell me what you want to know more about, or weigh in on the latest Moneyist columns.

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My wife has a degenerative neurological disease. My father-in-law wants to put her in a facility and take over our finances - MarketWatch

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Deep Brain Stimulation: The Answer to Chronic Pain? – Neurology Advisor

Chronic pain affects 1 in every 4 adults in the United States, many of whom are resistant to pharmacotherapy.1 It is a significant burden to both individuals and healthcare systems, affecting mental health, cognitive function, and promoting opioid dependency.2 However, researchers are hot on the heels of discovering new ways to treat the condition including via deep brain stimulation (DBS).

What is DBS?

DBS has the potential to treat a variety of neurological diseases by the implantation of electrical leads into specific areas of the brains cortex or subcortex, linking the leads to an implanted electrical stimulator.3 The appropriate areas of the brain are then stimulated with electrical current to ease or eliminate certain symptoms. While this treatment strategy is approved for motor diseases like essential tremors, dystonia, and Parkinsons disease, it is gaining increasing interest for pain relief in therapy-resistant individuals.4

DBS for the treatment of chronic pain

Since the 1950s, researchers have investigated DBS for the treatment of individuals with incurable, pain-inducing disorders.5 These investigations involved a variety of intractable pain syndromes, ranging from brachial plexopathy, injury of the spinal cord, and thalamic pain syndrome, to accident-related pain and mechanical lower back pain.6 Success has also been reported for incurable facial pain, although subsequent studies targeting different chronic pain disorders demonstrated inconsistent efficacy.5,6 Consequently, DBS is still considered investigational and off-label for chronic pain treatment today.

This off-label status has not hindered research, however. One study reported the results of 59 patients with a diverse range of chronic pain syndromes, who received DBS in the periventricular grey (PVG) area of the brain and/or the thalamus.7 In comparison to pre-operative levels, results indicated a drastic improvement, with more than half of patients, regardless of pain etiology, reporting pain relief by 50 percent.

Another study involved performing DBS on the periaqueductal grey (PAG) or PVG area, along with the sensory region of the thalamus or internal capsule, on patients with a variety of pain etiologies. Pain reduction exceeded 50 percent.8

Interestingly, some patients who fail to meet the 50 percent pain reduction criteria so often used in research testify to being greatly satisfied with any amount of pain reduction as it significantly improves their quality of life.9 This means that many patients are documented to have failed DBS treatment regardless of a partial, but notable, improvement.

Identifying novel target sites for chronic pain therapy

According to Prasad Shirvalkar, pain physician and Assistant Professor at the University of California, Historically, DBS has overwhelmingly targeted two brain regions: the ventral thalamus and the PAG areas. Thalamic DBS was hypothesized to work consistent with the Gate Control Theory of pain. It is believed that stimulating the thalamus produces tingling or other paraesthesia that effectively block pain-related transmission from fibers that provide input from the periphery and spinal cord. The Gate Control Theory posits that ascending fibers/inputs to the brain have limited bandwidth, and that providing some additional input may interfere with pain signal transmission. The PAG DBS may help by boosting the bodys endogenous opioid system, but there is some controversy over this.3

According to research, a low frequency below 50 Hz is presumed to have an analgesic effect upon thalamus and PAG stimulation, while higher frequencies above 70 Hz are presumed to increase pain sensitivity. Additionally, stimulation of the ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei causes a pleasant sensation that overrides pain, while stimulation of PVG and PAG areas triggers analgesia and a warm sensation over the painful region.9

More recently, a team at Oxford has introduced DBS of the anterior cingulate cortex (ACC), which may dampen the unpleasantness or bothersomeness of pain without affecting the somatosensory component of pain, says Shirvalkar. Patients have reported that even though pain was not totally relieved, it was less irritating or felt distant from them, demonstrating the emotional or affective aspect of the ACC.9

Overcoming barriers to the effective use of DBS

DBS currently involves a constant flow of electrical current and does not adjust to changes in brain activity.1 According to Shirvalkar, One of the biggest obstacles with DBS for pain is that no matter which target is stimulated, DBS often loses effect in the long term over 1-2 years for many patients. That is, the brain seems to adapt to the stimulation and ignores it. We are trying to figure out how to overcome such adaptation.3

It is more likely that multiple brain regions conspire over a network to produce and perpetuate chronic pain states, Shirvalkar explains. We are conducting a clinical trial that incorporates a novel trial period, where patients temporarily have electrodes placed in their brain for a period of 10 days. We then work very hard over 10 days to record brain activity and stimulate multiple regions that we believe are important for chronic pain. This way, we can determine which sites or nodes are most pain-relieving when stimulated for that individual person. By performing a comprehensive trial period, Shirvalkar and his team can learn more about the network behavior of chronic pain in the brain and maximize the probability of finding an efficacious therapy for each patient. Importantly, Shirvalkar says, This way, patients are not implanted with a permanent device when there is a low chance of long-term benefit.

Any emerging research findings could advance treatment for other conditions too. Other brain diseases that are treated with brain stimulation such as epilepsy, Parkinsons disease, and depression (although experimentally) could also benefit from developing technology where stimulation responds to ongoing neural activity, says Shirvalkar. Many of my colleagues are working on developing adaptive DBS for these other medical conditions.

The future of DBS for chronic pain

Going forward, Shirvalkar believes that there is the need for advancement in two key scientific areas. The first is understanding basic brain mechanisms that underlie these diseases so that we can better understand what effect stimulation is actually having on the disease itself, he says. The second is figuring out how we can modulate the key brain circuits non-invasively, using transcranial magnetic stimulation or scalp stimulation. I think the future is moving away from stimulating single brain regions and towards networks, ultimately with the goal of doing this without invasive implants.

References

1. Miller, JA. Tailoring deep brain stimulation to treat chronic pain. UC San Francisco. Published February 3, 2020. Accessed December 20, 2020. https://www.ucsf.edu/news/2020/02/416601/tailoring-deep-brain-stimulation-treat-chronic-pain.

2. Dydyk AM, Yarrarapu SNS, Conermann T. Chronic Pain. StatPearls; 2020. Updated November 8, 2020. https://www.ncbi.nlm.nih.gov/books/NBK553030/

3. Shirvalkar P, Sellers KK, Schmitgen A, et al. A Deep Brain Stimulation Trial Period for Treating Chronic Pain. J Clin Med. 2020;9(10):3155. doi:10.3390/jcm9103155

4. Lozano AM, Lipsman N, Bergman H, et al. Deep brain stimulation: current challenges and future directions. Nat Rev Neurol. 2019;15(3):148-160. doi:10.1038/s41582-018-0128-2

5. Frizon LA, Yamamoto EA, Nagel SJ, Simonson MT, Hogue O, Machado AG. Deep Brain Stimulation for Pain in the Modern Era: A Systematic Review. Neurosurgery. 2020;86(2):191-202. doi:10.1093/neuros/nyy552

6. Ben-Haim S, Mirzadeh Z, Rosenberg WS. Deep brain stimulation for intractable neuropathic facial pain. Neurosurg Focus. 2018;45(2): E15. doi:10.3171/2018.5.FOCUS18160

7. Boccard SGJ, Pereira EAC, Moir L, Aziz TZ, Green AL Long-term outcomes of deep brain stimulation for neuropathic pain. Neurosurgery. 2013; 72:221-230. doi:10.1227/NEU.0b013e31827b97d6

8. Kumar K, Toth C, Nath RK Deep brain stimulation for intractable pain: A 15-year experience. Neurosurgery. 1997; 40:736-746. doi:10.1097/00006123-199704000-00015

9. Farrell SM, Green A, Aziz T. The Current State of Deep Brain Stimulation for Chronic Pain and Its Context in Other Forms of Neuromodulation. Brain Sci. 2018;8(8):158. doi:10.3390/brainsci8080158

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Recurrent GBM brain tumors with few mutations respond best to immunotherapy – Duke Department of Neurology

Glioblastoma brain tumors are especially perplexing. Inevitably lethal, the tumors occasionally respond to new immunotherapies after theyve grown back, enabling up to 20% of patients to live well beyond predicted survival times.

What causes this effect has long been the pursuit of researchers hoping to harness immunotherapies to extend more lives.

New insights from a team led by Dukes Preston Robert Tisch Brain Tumor Center, including Katherine Peters, MD, PhD, Dina Randazzo, DO, and Annick Desjardins, MD provide potential answers. The team found that recurring glioblastoma tumors with very few mutations are far more vulnerable to immunotherapies than similar tumors with an abundance of mutations.

The finding, appearing online Jan. 13 in the journal Nature Communications, could serve as a predictive biomarker to help clinicians target immunotherapies to those tumors most likely to respond. It could also potentially lead to new approaches that create the conditions necessary for immunotherapies to be more effective.

Its been frustrating that glioblastoma is incurable and weve had limited progress improving survival despite many promising approaches, said senior author David Ashley, MD, PhD, professor in the departments of Neurosurgery, Medicine, Pediatrics and Pathology at Duke University School of Medicine.

Weve had some success with several different immunotherapies, including the poliovirus therapy developed at Duke, Ashley said. And while its encouraging that a subset of patients who do well when the therapies are used to treat recurrent tumors, about 80% of patients still die.

Ashley and colleagues performed genomic analyses of recurrent glioblastoma tumors from patients treated at Duke with the poliovirus therapy as well as others who received so-called checkpoint inhibitors, a form of therapy that releases the immune system to attack tumors.

In both treatment groups, patients with recurrent glioblastomas whose tumors had few mutations survived longer than the patients with highly mutated tumors. This was only true, however, for patients with recurrent tumors, not for patients with newly diagnosed disease who had not yet received treatment.

This suggests that chemotherapy, which is the standard of care for newly diagnosed glioblastoma, might be altering the inflammatory response in these tumors, Ashley said, adding that chemotherapy could be serving an important role as a primer to trigger an evolution of the inflammation process in recurrent tumors.

Ashley said the finding in glioblastoma could also be relevant to other types of tumors, including kidney and pancreatic cancers, which have similarly shown a correlation between low tumor mutations and improved response to immunotherapies.

In addition to Ashley, study authors include Matthias Gromeier, Michael C. Brown, Gao Zhang, Xiang Lin, Yeqing Chen, Zhi Wei, Nike Beaubier, Hai Yan, Yiping He, Annick Desjardins, James E. Herndon II, Frederick S. Varn, Roel G. Verhaak, Junfei Zhao, Dani P. Bolognesi, Allan H. Friedman, Henry S. Friedman, Frances McSherry, Andrea M. Muscat, Eric S. Lipp, Smita K. Nair, Mustafa Khasraw, Katherine B. Peters, Dina Randazzo, John H. Sampson, Roger E. McLendon and Darell D. Bigner.

The study received support from The Brain Tumor Research Charity, Jewish Communal Fund, Circle of Service Foundation, Uncle Kory Foundation, Department of Defense (W81XWH-16-1-0354) and the National Institutes of Health (R35CA197264, P01CA154291, P50CA190991, R01NS108773, R01NS099463, R21NS112899, P01CA225622, F32CA224593). Support was also received through the Angels Among Us fundraising event and a gift from the Asness Family.

Authors Gromeier, Brown, Desjardins, Bolognesi, Henry Friedman, Nair, Sampson, Bigner and Ashley own intellectual property related to the poliovirus therapy, which has been licensed to Istari Oncology, Inc. Gromeier, Desjardins, Bolognesi, Allan Friedman, Henry Friedman and Bigner hold equity in Istari Oncology, Inc. Additional disclosures are provided in the published study.

This story originally appeared on the Duke Health website. View it in its original location here.

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Type of Alzheimer’s With Intact Memory Offers New Research Paths – Medscape

Patients with a rare type of Alzheimer's disease do not show the memory loss characteristic of the condition even over the long term, new research suggests. They also show some differences in neuropathology to typical Alzheimer's patients, raising hopes of discovering novel mechanisms that might protect against memory loss in typical forms of the disease.

Dr Marsel Mesulam

"We are discovering that Alzheimer's disease has more than one form. While the typical Alzheimer's patient will have impaired memory, patients with primary progressive aphasia linked to Alzheimer's disease are quite different. They have problems with language they know what they want to say but can't find the words but their memory is intact," lead author Marsel Mesulam, MD, told Medscape Medical News.

"We have found that these patients still show the same levels of neurofibrillary tangles which destroy neurons in the memory part of the brain as typical Alzheimer's patients, but in patients with primary progressive aphasia Alzheimer's the nondominant side of this part of the brain showed less atrophy," added Mesulam, who is director of the Mesulam Center for Cognitive Neurology and Alzheimer's Disease at Northwestern University Feinberg School of Medicine, Chicago, Illinois. "It appears that these patients are more resilient to the effects of the neurofibrillary tangles."

The researchers also found that two biomarkers that are established risk factors in typical Alzheimer's disease do not appear to be risk factors for the primary progressive aphasia (PPA) form of the condition.

"These observations suggest that there are mechanisms that may protect the brain from Alzheimer's-type damage. Studying these patients with this primary progressive aphasia form of Alzheimer's may give us clues as to where to look for these mechanisms that may lead to new treatments for the memory loss associated with typical Alzheimer's disease," Mesulam commented.

The study was published online in the January 13 issue of Neurology.

PPA is diagnosed when language impairment emerges on a background of preserved memory and behavior, with about 40% of cases representing atypical manifestations of Alzheimer's disease, the researchers explain.

"While we knew that the memories of people with primary progressive aphasia were not affected at first, we did not know if they maintained their memory functioning over years," Mesulam noted.

The current study aimed to investigate whether the memory preservation in PPA linked to Alzheimer's is a consistent core feature or a transient finding confined to initial presentation, and to explore the underlying pathology of the condition.

The researchers searched their database to identify patients with PPA with autopsy or biomarker evidence of Alzheimer's, who also had at least two consecutive visits during which language and memory assessment had been obtained with the same tests.

The study included 17 patients with the PPA-type Alzheimer's disease. They were compared with 14 patients who had typical Alzheimer's disease with memory loss.

The authors point out that characterization of memory in patients with PPA is challenging because most tests use word lists, and thus patients may fail the test because of their language impairments. To address this issue, they included patients with PPA who had had memory tests involving recalling pictures of common objects.

Patients with typical Alzheimer's disease underwent similar tests but used a list of common words.

A second round of tests was conducted in the primary progressive aphasia group an average of 2.4 years later and in the typical Alzheimer's group an average of 1.7 years later.

Brain scans were also available for the patients with PPA, as well as postmortem evaluations for eight of the PPA cases and all the typical Alzheimer's cases.

Results showed that patients with PPA had no decline in their memory skills when they took the tests a second time. At that point, they had been showing symptoms of the disorder for an average of 6 years. In contrast, their language skills declined significantly during the same period. For typical Alzheimer's patients, verbal memory and language skills declined with equal severity during the study.

Postmortem results showed that the two groups had comparable degrees of Alzheimer's pathology in the medial temporal lobe the main area of the brain affected in dementia.

However, MRI scans showed that patients with PPA had an asymmetrical atrophy of the dominant (left) hemisphere with sparing of the right sided medial temporal lobe, indicating a lack of neurodegeneration in the nondominant hemisphere, despite the presence of Alzheimer's pathology.

It was also found that the patients with PPA had significantly lower prevalence of two factors strongly linked to Alzheimer's TDP-43 pathology and APOE 4 positivity than the typical Alzheimer's patients.

The authors conclude that: "Primary progressive aphasia Alzheimer's syndrome offers unique opportunities for exploring the biological foundations of these phenomena that interactively modulate the impact of Alzheimer's neuropathology on cognitive function."

In an accompanying editorial, Seyed Ahmad Sajjadi, MD, University of California, Irvine; Sharon Ash, PhD, University of Pennsylvania, Philadelphia; and Stefano Cappa, MD, University School for Advanced Studies, Pavia, Italy, say these findings have important implications, "as ultimately, preservation of cognition is the holy grail of research in this area."

They point out that the current observations imply "an uncoupling of neurodegeneration and pathology" in patients with PPA-type Alzheimer's, adding that "it seems reasonable to conclude that neurodegeneration, and not mere presence of pathology, is what correlates with clinical presentation in these patients."

The editorialists note that the study has some limitations: the sample size is relatively small; not all patients with PPA-type Alzheimer's underwent autopsy; MRI was only available for the aphasia group; and the two groups had different memory tests for comparison of their recognition memory.

But they conclude that this study "provides important insights about the potential reasons for differential vulnerability of the neural substrate of memory in those with different clinical presentations of Alzheimers pathology."

The study was supported by the National Institute on Deafness and Communication Disorders, the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the Davee Foundation, and the Jeanine Jones Fund.

Neurol. Published online January 13, 2021. Abstract, Editorial

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