Diagnosis .
LANS likelihoods (only including patients with all features available) . | ||||
---|---|---|---|---|
Mayo cohort Diagnosis . | Low . | Moderate . | High . | Highest . |
ADNC | 31 | 17 | 1 | 0 |
ADNC/LATE-NC | 12 | 8 | 13 | 0 |
LATE-NC | 0 | 0 | 2 | 2 |
Standard and advanced LANS features . | ||||||
---|---|---|---|---|---|---|
ADNI cohort . | Age ≥75 . | Mild syndrome . | Hippocampal atrophy . | Limbic hypometabolism . | Absence of neocortical hypometabolism . | Low neocortical tau likelihood . |
ADNC | 15/26 | 20/26 | 11/26 | 1/18 | 2/18 | 1/22 |
ADNC/LATE-NC | 12/19 | 12/19 | 15/19 | 4/13 | 1/13 | 0/17 |
LATE-NC | 4/8 | 8/8 | 5/8 | 5/6 | 1/6 | 8/8 |
Standard and advanced LANS features . | ||||||
---|---|---|---|---|---|---|
ADNI cohort . | Age ≥75 . | Mild syndrome . | Hippocampal atrophy . | Limbic hypometabolism . | Absence of neocortical hypometabolism . | Low neocortical tau likelihood . |
ADNC | 15/26 | 20/26 | 11/26 | 1/18 | 2/18 | 1/22 |
ADNC/LATE-NC | 12/19 | 12/19 | 15/19 | 4/13 | 1/13 | 0/17 |
LATE-NC | 4/8 | 8/8 | 5/8 | 5/6 | 1/6 | 8/8 |
LANS likelihoods (only including patients with all features available) . | ||||
---|---|---|---|---|
Diagnosis . | Low . | Moderate . | High . | Highest . |
ADNC | 11 | 7 | 0 | 0 |
ADNC/LATE-NC | 8 | 3 | 1 | 0 |
LATE-NC | 2 | 0 | 1 | 3 |
LANS likelihoods (only including patients with all features available) . | ||||
---|---|---|---|---|
Diagnosis . | Low . | Moderate . | High . | Highest . |
ADNC | 11 | 7 | 0 | 0 |
ADNC/LATE-NC | 8 | 3 | 1 | 0 |
LATE-NC | 2 | 0 | 1 | 3 |
LANS, limbic-predominant amnestic neurodegenerative syndrome; ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-related TDP-43 encephalopathy neuropathological changes.
In the Mayo cohort, all LATE-NC (4/4) patients had a highest/high likelihood. Thirty-one of forty-nine (63%), 17/49 (35%) and 1/49 (2%) of ADNC patients had low, moderate and highest/high likelihoods, respectively. Twelve of thirty-three (36%), 8/33 (24%) and 13/33 (39%) of ADNC/LATE-NC patients had low, moderate and highest/high likelihoods, respectively. Assessments of the distribution of pathological diagnoses within likelihood categories revealed that there were proportionally more ADNC/LATE-NC than ADNC patients within the highest/high likelihood category ( P = 0.007). There were more ADNC and ADNC/LATE-NC patients than LATE-NC patients within the moderate likelihood category ( P < 0.001 and P = 0.02, respectively). There were more ADNC and ADNC/LATE-NC patients than LATE-NC patients ( P = 0.004) and more ADNC patients than ADNC/LATE-NC patients ( P < 0.001) within the low likelihood category. Assessment of the distribution of likelihood categories within pathological diagnoses revealed that there were more ADNC patients with low and moderate likelihoods compared to highest/high likelihoods ( P < 0.001 and P = 0.002, respectively). There were no other differences.
In the ADNI cohort, 4/6 (67%) and 2/6 (33%) of LATE-NC cases had highest/high and low likelihoods, respectively. Eleven of eighteen (61%) and 7/18 (39%) of ADNC cases had low and moderate likelihoods, respectively. Eight of twelve (67%), 3/12 (25%) and 1/12 (8%) of ADNC/LATE-NC patients had low, moderate and highest/high likelihoods, respectively. Assessments of the distribution of pathological diagnoses within likelihood categories only revealed a trend towards more ADNC patients than LATE-NC patients within the moderate likelihood category ( P = 0.09). Assessment of the distribution of likelihood categories within pathological diagnoses revealed that there were more ADNC patients with a low likelihood compared to highest/high likelihoods ( P = 0.04). There were no other differences.
Assessment of longitudinal trajectories of CDR-SB according to LANS likelihood and FDG-PET findings comparing LANS likelihoods to CUs are displayed in Fig. 3 . Results from mixed linear modelling between longitudinal CDR-SB and LANS likelihoods are in Supplementary Table 4 . This analysis showed that all groups had equivalent CDR-SB scores at baseline. LANS likelihoods differed in their CDR-SB trajectory over time in that patients with a high likelihood had a slower increase of CDR-SB score than those with a low likelihood. There were trends towards significance for a slower increase of CDR-SB scores in patients with a high likelihood compared to those with moderate and low likelihoods.
FDG-PET and longitudinal CDR-SB findings across LANS likelihoods. ( A ) FDG-PET findings comparing LANS likelihoods to CUs. Contrasts were generated using SPM12 using pairwise t -comparisons between groups at the voxel level and involved 42 cases with a low likelihood, 25 cases with a moderate likelihood, 15 cases with a highest/high likelihood and 112 CUs. ( B ) Longitudinal CDR-SB trajectories at the individual and group level are displayed on the right. CU, cognitively unimpaired; FDR, false discovery rate; CDR-SB, Clinical Dementia Rating Scale Sum of Boxes.
FDG-PET findings showed that patients with highest/high likelihoods had patterns of degeneration mostly involving the temporo-limbic system and inferior frontal areas with little involvement of neocortical areas compared to CUs. In contrast, those with a low likelihood had more pronounced neocortical degeneration mostly involving lateral temporo-parietal areas with little involvement of the medial temporal lobe. The moderate likelihood showed a mixture of these patterns, with involvement of both medial temporo-limbic and neocortical areas.
A logistic model classifying patients with (LATE-NC, ADNC/LATE-NC) or without LATE-NC (ADNC) based on operationalized LANS criteria (age at examination, CDR-SB score, hippocampal volume, IMT ratio, FDG-PET meta-ROI, tau positivity) achieved a balanced accuracy of 74.6% in the Mayo cohort. The sensitivity and specificity of the model were 78.6 and 70.6%, respectively. There were 12/15 (80%) true positives (i.e. correctly classified with LATE-NC) and 11/16 (68.75%) true negatives (i.e. correctly classified without LATE-NC). Out-of-sample predictions in the ADNI cohort using the model fitted in the Mayo cohort achieved a balanced accuracy of 73.3% in the ADNI cohort. The sensitivity and specificity of the model were 60.9 and 85.7%, respectively. There were 9/15 (60%) true positives (i.e. correctly classified with LATE-NC) and 14/15 (93.33%) true negatives (i.e. correctly classified without LATE-NC). A qualitative assessment of age and CDR-SB scores in misclassified cases showed that false positive (predicted to have LATE-NC whereas they did not) were older and less impaired than ADNC cases (i.e. true negatives) and that false negatives (predicted not to have LATE-NC whereas they did) were younger and more impaired than ADNC/LATE-NC and LATE-NC cases (i.e. true positives). While these comparisons were not statistically significant, this suggests that these cases may have mixed clinical features and are not representative of the archetypical profiles of ADNC or LATE-NC, respectively.
We conducted an exploratory analysis on the clinical heterogeneity of ADNC/LATE-NC patients on the premise that some have LATE-NC as a primary pathology and ADNC as a co-pathology and vice versa. We stratified ADNC/LATE-NC patients based on their LANS likelihood into highest/high ( n = 13), moderate ( n = 8) and low ( n = 12) likelihoods. This was only done in the Mayo cohort given the relatively low heterogeneity of LANS likelihoods in ADNC/LATE-NC patients from the ADNI cohort. Results from these analyses are visually depicted in Fig. 4 .
FDG-PET and longitudinal CDR-SB findings in ADNC/LATE-NC according to LANS likelihoods relative to other groups. ( A ) FDG-PET findings comparing ADNC/LATE-NC to CUs. Contrasts were generated using SPM12 using pairwise t -comparisons between groups at the voxel level and involved 12 ADNC/LATE-NC cases with a low likelihood, 8 ADNC/LATE-NC cases with a moderate likelihood, 13 ADNC/LATE-NC cases with a high/highest likelihood and 112 CUs. ( B ) Longitudinal CDR-SB trajectories at the individual and group level are displayed on the right. ADNCs, Alzheimer’s disease neuropathological changes; LATE-NCs, limbic-predominant age-associated TDP-43 encephalopathy pathological changes; CU, cognitively unimpaired; FDR, false discovery rate; CDR-SB, Clinical Dementia Rating Scale Sum of Boxes.
Results from the mixed linear model assessing the longitudinal trajectory of CDR-SB scores according to time since baseline across groups (ADNC, ADNC/LATE-NC highest/high, ADNC/LATE-NC moderate, ADNC/LATE-NC low, LATE-NC) are in Supplementary Table 5 . This analysis showed that all groups had statistically equivalent CDR-SB scores at baseline. Groups differed in their CDR-SB trajectory over time in that ADNC/LATE-NC patients with a low likelihood had a steeper increase in CDR-SB scores compared to all other groups.
FDG-PET findings showed that ADNC/LATE-NC patients with highest/high likelihoods had patterns of degeneration mostly involving the temporo-limbic system with little involvement of neocortical areas aside from the inferior frontal areas compared to CUs. In contrast, ADNC/LATE-NC patients with a low likelihood had more pronounced neocortical degeneration mostly involving lateral temporo-parietal areas with lesser involvement of the medial temporal lobe. ADNC/LATE-NC patients with a moderate likelihood showed an intermediate pattern, with involvement of both medial temporo-limbic and neocortical areas.
We developed a set of clinical criteria to identify individuals with a predominant and progressive amnestic syndrome driven by degeneration of the temporo-limbic system. We termed this clinical entity LANS to emphasize that it does not necessarily have a strict mapping to LATE-NC even though they share limbic predominance. This neurologic condition is characterized by progressive limbic degeneration and associated clinical signs and symptoms requiring comprehensive evaluation including history, physical, neuropsychological assessment, imaging and fluid biomarkers. Various combinations of neuropathologies like LATE-NC, ADNC, LBD, argyrophilic grain disease and PART have been observed in the setting of this neurologic syndrome. We operationalized and validated the LANS criteria by tying limbic degeneration to an older age at evaluation, mild clinical syndrome, disproportionate hippocampal atrophy according to clinical severity, limbic hypometabolism, absence of neocortical degenerative disease pattern and low likelihood of neocortical tau. The LANS criteria effectively categorized LATE-NC, ADNC/LATE-NC and ADNC patients from two clinicopathological cohorts (Mayo and ADNI). Most patients with highest or high LANS likelihoods had post-mortem evidence of LATE-NC, most patients with moderate or low LANS likelihoods had evidence of ADNC, and those with evidence of ADNC/LATE-NC patients had a wider distribution of LANS likelihoods. Assessing clinical and imaging features across LANS likelihood regardless of underlying pathology showed that patients with higher likelihoods had a slower clinical course and patterns of temporo-limbic degeneration with minimal involvement of neocortical areas, while those with lower likelihoods showed the opposite pattern. Stratifying ADNC/LATE-NC patients according to their LANS likelihoods revealed a high degree of heterogeneity, where those with higher likelihoods had a slower clinical course and those with lower likelihood had the worse clinical prognosis compared to all other groups. The implementation of LANS criteria has critical implications for clinical and therapeutic endeavours as well as for a deeper understanding of the aetiologic landscape of predominant and progressive amnestic syndromes.
Patients with LATE-NC had a mild level of cognitive impairment at presentation with relatively slow progression of impairment over time, which further consolidates findings from separate studies findings a memory-dominant profile characterized by an indolent clinical course in LATE-NC. 1 , 3 , 6 , 70 Interestingly, patients with ADNC/LATE-NC with a high LANS likelihoods showed a relatively similar profile in terms of clinical progression, which aligns with our hypothesis that these patients have LATE-NC as the primary driver of their clinical symptoms with ADNC as a secondary pathology. This is further supported by the finding of a more rapid clinical decline in ADNC/LATE-NC patients with a low LANS likelihood, which are hypothesized to have ADNC as the primary driver of their clinical symptoms and may thus have combined limbic and neocortical functional neurodegeneration. These findings bring nuance to the prevailing view that patients with evidence for both pathologies systematically have worse clinical outcomes than ADNC alone. 6 , 70 They also allow for the prediction of the primary symptom-driving pathology in vivo in the context of comorbidity.
FDG-PET and MRI imaging results are also indicative of a selective degeneration of the limbic system including strong involvement of the hippocampus associated with LATE-NC, above and beyond the contribution of ADNC. In fact, ADNC was significantly associated with degeneration of the lateral temporal lobe and posterior neocortical areas rather than the limbic system. This aligns well with previous studies assessing imaging features of LATE-NC and/or ADNC. 24 , 25 , 28-31
The proposed LANS criteria have several clinical implications. The primary implication of these criteria is to accurately diagnose patients for whom the cause of progressive and predominant amnestic symptoms is linked to the degeneration of the limbic system with a high likelihood of LATE-NC as a symptom-driving pathology. It is noteworthy that the diagnosis of LANS is based on likelihoods, and not on definitive categories as seen with other classifications. This means that the unavailability of some features does not preclude rendering LANS diagnosis. Rather, it prevents from reaching higher LANS likelihoods and prompts further workup to ascertain that symptoms are caused by predominant limbic degeneration. This underlines the critical role of imaging and biomarkers to increase the diagnostic confidence of LANS. Figure 5 demonstrates a prospective example of clinical case of LANS, where a moderate likelihood was assigned based upon the assessment of core and standard features. The assessment of advanced features (negative amyloid-PET, predominant limbic hypometabolism on FDG-PET) increased confidence that limbic degeneration was the culprit of symptoms, thus allowing for the highest LANS likelihood.
Case example of a prospective use of the LANS criteria in clinical settings. This patient was seen at Mayo Clinic, Rochester, to determine eligibility for an anti-amyloid monoclonal antibody therapy, and the LANS criteria were internally defined at the time of evaluation. The criteria were operationalized using clinical judgement of available data including visual reads of neuroimaging as is the current standard in clinical practice. This patient was a female over the age of 75 with a history of memory problems for several years. She lived alone, managed her instrumental activities of daily living independently and was still working part-time. Neuropsychological testing revealed moderate to severe impairment on measures of delayed recall and fragility of salient semantic knowledge (i.e. she could not recall details about the events occurring on 11 September 2001; she named another building than the World Trade Center and did not know how many buildings were hit). Performance was also mildly low on a task of object naming. The remainder of the assessment (i.e. global cognition, executive functions, visuospatial processing and language) was within or above expectations from a normative standpoint. The profile was consistent with single-domain amnestic mild cognitive impairment. MRI revealed disproportionate bilateral hippocampal atrophy, and she was assigned a moderate likelihood LANS diagnosis. Subsequently, a brain FDG-PET revealed prominent temporo-limbic and milder inferior frontal hypometabolism in the absence of a neocortical degenerative pattern by visual read. Amyloid-PET was read as negative. She thus met all core, standard and advanced criteria for LANS, corresponding to the highest likelihood. She did not meet criteria for an anti-amyloid monoclonal antibody therapy and was counselled about diagnosis, prognosis and most likely underlying aetiology.
The accurate diagnosis of LANS has the potential to improve prognostication and counselling of patients about the nature of their symptoms. Current evidence indicates that the symptomatology primarily involves episodic memory for recent events, while neocortical functions (e.g. executive functioning and visuospatial reasoning) are expected to remain relatively preserved throughout the disease course. 1 , 2 , 19 An accurate diagnosis is also relevant for prognostication, as LANS has a likelihood of being associated with LATE-NC, which is associated with a relatively slow and milder clinical course compared to canonical Alzheimer’s disease–type dementia per our results and other studies. 1 , 3 , 6 , 70 This is again exemplified in Fig. 5 , where a highest LANS likelihood allowed to have precise diagnosis, counsel prognosis, guide treatment options and provide answers about the mostly likely underlying aetiology in this patient allowing for engagement with research and other health information on this topic. Without a LANS construct, we are left only saying that a patient does not qualify for anti-amyloid treatment and that they do not have Alzheimer’s disease. Having a positive diagnosis serves additional utility beyond that and facilitates comprehensive medical care.
To put this work in contexts, recent work on terminology would characterize LANS as a subtype of amnestic MCI or amnestic dementia. 34 , 35 The addition of preservation of neocortical functions, older age at symptom onset, mild clinical severity and semantic memory impairment would make these amnestic syndromes more likely to be LANS and the additional imaging would localize the syndromes to the limbic system. These refinements would add greater specificity to the diagnosis for clinicians. LANS in the context of normal amyloid levels can also be examined through the lens of suspected non–Alzheimer disease pathophysiology, which refers to amyloid-negative, neurodegeneration-positive individuals. 71 However, suspected non–Alzheimer disease pathophysiology encompasses a broader spectrum of conditions than LANS, as it is a biomarker-based definition regardless of clinical status.
The LANS criteria have critical therapeutic implications. This is especially true in this era of emerging anti-amyloid monoclonal antibody therapies. 32 , 33 , 72 , 73 As these therapies make their way into clinical practice, the LANS criteria can be of relevance for identifying patients with a high likelihood of LATE-NC as the primary cause of their symptoms and guide clinical decision-making and counselling regarding potential therapeutic avenues. It is important to mention that positive Alzheimer’s disease biomarkers do not rule out a diagnosis of LANS, as a progressive and predominant amnestic syndrome caused by LATE-NC or other pathologies can be observed in concomitance with incidental amyloidosis or ADNC. 30 , 31 The use of the LANS likelihoods can help determine whether the amnestic syndrome is most likely driven by a primary non–Alzheimer disease pathophysiology with secondary ADNC or vice versa, as demonstrated by our analysis deciphering the heterogeneity of patients with ADNC/LATE-NC. It is important to mention that we do not make treatment recommendations based on this work, but the LANS criteria allow to study such a question. Future studies will be important to determine how patients with positive Alzheimer’s disease biomarkers respond to disease-modifying therapies according to their LANS likelihood. Finally, the LANS criteria are a major advancement in the overarching goal of tying an in vivo neurologic syndrome to underlying LATE-NC. The other critical component needed to achieve this is the development of in vivo diagnostic biomarkers of TDP-43 specific for LATE-NC. PET, CSF and biofluid biomarkers of TDP-43 are hopefully on the horizon. 1 , 74 , 75 This would allow for defining the clinical entity of LATE as a high-likelihood LANS syndrome with biomarker evidence of LATE-NC. Defining such a clinicopathological entity will be important for the design of clinical trials aimed at LATE-NC in terms of defining eligibility criteria and outcomes measures.
It is important to reiterate that while LANS is highly associated with LATE-NC, it can be associated with other pathologic entities that selectively target the limbic system. Supplemental analyses provide some evidence that pathologies associated with a predominant amnestic syndrome other than LATE-NC may, in rare instances, have a high LANS likelihood (e.g. LBD, argyrophilic grain disease, advanced PART). One example that can be a potential source of clinical conundrums is the limbic variant Alzheimer’s disease, where tau predominantly localizes to the limbic system and therefore qualifies for LANS. In this scenario, the advanced LANS criteria in combination with visual assessment of tau-PET can help in determining which pathology has the highest likelihood of driving clinical symptoms.
Notably, there were slightly lower LANS likelihoods in ADNC/LATE-NC patients in the ADNI cohort relative to the Mayo cohort. This is likely due to discrepancy in recruitment and sampling strategies. The Mayo cohort draws from clinical practice in a tertiary behavioural neurology clinic (Alzheimer’s Disease Research Center) and randomly selected individuals living in Olmsted County, MN, USA (Mayo Clinic Study of Aging). 76 It is thus designed to reflect a combination of the clinicopathologic variability encountered in Alzheimer’s disease–oriented clinical context and with more representative settings. On the other hand, ADNI was designed as a research cohort aimed at the clinical and biological characterization of individuals on the clinicopathologic spectrum of Alzheimer’s disease. 77 , 78 It is not meant to reflect the heterogeneity encountered in clinical practice. These fundamental differences may explain the relatively younger age of LATE-NC patients and the lower frequency of ADNC/LATE-NC with a high LANS likelihood. We believe the performance of the LANS criteria in the Mayo cohort is a more accurate reflection of how the LANS criteria are expected to perform in clinical settings. It is also important to mention that we undertook several steps to avoid overfitting the LANS criteria validation in the Mayo cohort. This includes the use of externally validated thresholds for most imaging and tau biomarkers (e.g. CSF, ptau181, molecular PET imaging) and deriving optimal thresholds for hippocampal atrophy and the IMT ratio in the ADNI cohort rather than Mayo.
There are some limitations to this work. An evident caveat is the low number of patients with LATE-NC without ADNC. The lack of statistical differences between these patients and other groups in terms of clinical and imaging features could be attributable to the small sample size rather than a genuine absence of differences. However, most patients with LATE-NC had highest and high LANS likelihoods, suggesting that our proposed criteria effectively identify these individuals. Although the proposed LANS criteria include impaired semantic memory, we did not incorporate this feature in the operationalized criteria given the less robust and variably defined evidence of such impairment. Efforts are underway to better characterize the nature and extent of semantic memory impairment in patients with LATE-NC and develop cognitive tests sensitive to such impairment. This should not, however, prevent clinicians from considering this feature in their clinical decision-making when LANS is in the differential, as highlighted in the case example in Fig. 5 . The classification model based on the features of the LANS criteria had modest accuracy in distinguishing LATE-NC from ADNC at autopsy, which may be due to a range of factors including increased pathological burden in late-stage disease and partially overlapping clinical and radiological features between the two pathological entities. Prospective studies are required to further assess the value of the LANS criteria in predicting underlying pathologies predominantly driving limbic versus neocortical degeneration. This study is retrospective in nature. The implementation of the LANS criteria in clinical settings and prospective studies are needed to further validate and refine this set of criteria. Finally, while we report vascular burden across both cohorts, this information was not utilized in assigning pathological diagnoses unless seen in isolation. Future work with sample allowing for such stratification is required to assess how vascular damage influences the clinical trajectory and pathophysiology of LANS.
In conclusion, we developed and validated a set of criteria for LANS designed to be used in clinical practice to identify individuals with a predominant amnestic syndrome driven by the degeneration of the temporo-limbic system with a high likelihood of underlying LATE-NC. This has important clinical implications including differential diagnosis with other common causes of episodic memory impairment such as neocortical degeneration driven by ADNC, counselling patients about the nature and course of their symptoms, providing appropriate treatments, referral to research programmes and the development of therapeutic efforts aimed at LATE-NC. Several steps lay ahead to improve the definition of LANS including the conduction of prospective studies and the development of clinical tools that are sensitive and specific to its cognitive features. Finally, the development of in vivo diagnostic markers of TDP-43 pathology is needed to embed LANS into a clinicopathological entity driven by LATE-NC, i.e. LATE.
Supplementary material is available at Brain Communications online.
We wish to thank our patients and their caregivers for their dedicated participation in our research programme. We would also wish to express our gratitude to all healthcare providers and research professionals who were involved in this study and patient care.
This work was funded in part by National Institutes of Health (NIH) grants P30 AG062677, P50 AG016574 and U01 AG006786 (R.C.P.) and R37 AG011378 and R01 AG041851 (C.R.J.), and by the Robert Wood Johnson Foundation, the Elsie and Marvin Dekelboum Family Foundation, the Liston Family Foundation, the Edson Family, the Gerald A. and Henrietta Rauenhorst (GHR) Foundation and the Foundation Dr. Corinne Schuler (Geneva, Switzerland).
V.J.L. consults for Bayer Schering Pharma, Piramal Life Sciences, Life Molecular Imaging, Eisai Inc., Avid Radiopharmaceuticals and Merck Research and receives research support from GE Healthcare, Siemens Molecular Imaging, Avid Radiopharmaceuticals and the NIH (NIA, NCI). D.S.K. serves on a Data Safety Monitoring Board for the DIAN study and for a tau therapeutic for Biogen but receives no personal compensation; is an investigator in clinical trials sponsored by Biogen, Lilly Pharmaceuticals and the University of Southern California; has served as a consultant for Roche, Samus Therapeutics, Third Rock and Alzeca Biosciences but receives no personal compensation; and receives funding from the NIH. B.F.B. receives honorarium for SAB activities for the Tau Consortium, is an investigator in clinical trials sponsored by Alector, Biogen, Cognition Therapeutics, EIP Pharma and Transposon and receives funding from the NIH. C.R.J. has no commercial conflicts and receives research support from the NIH, the GHR Foundation and the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic. R.C.P. consults for Roche, Inc.; Merck, Inc.; Biogen, Inc.; Genentech, Inc.; Eisai, Inc.; and Nestle, Inc. but does not receive significant fees due to NIH limitations from the U24 AG057437 Co-PI role.
Data from the Mayo Clinic Study of Aging and the Mayo Clinic Alzheimer’s Disease Research Center are available upon request ( https://www.mayo.edu/research/centers-programs/alzheimers-disease-research-center/data-requests ). ADNI data can be downloaded at https://adni.loni.usc.edu/ . The Mayo Clinic Adult Lifespan Template can be found at https://www.nitrc.org/projects/mcalt/ . The R code for the statistical analyses can be found on https://github.com/nickcorriveaul/R_scripts_manuscripts .
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When trying to prevent diseases, information is key, and if it’s reliable, all the better. With this new free medical template, you can show the results of a clinical case, including the symptoms, the patient monitoring, the treatment and all the important data. Its design will help you grab your audience’s attention for sure!
To begin with, the illustrations that we’ve included in the slides are so cool nobody will be able to take their eyes off the screen. These, along with the assortment of icons, demonstrate how good looking the flat style is. The next thing we should mention is color. The main protagonist in the slides design is blue, which is a color usually related to medical contexts. It’s not a surprise, since it conveys serenity and confidence; that’s exactly what you want to show in front of your audience, right? To make your titles readable and clear, a sans-serif font has been used. In fact, we’ve also chosen a sans-serif typeface for body text, but they are different enough and go well together. Don’t hesitate to make use of the graphs and infographics to explain in detail all the data gathered from your research. If you’re using Google Slides, then Flaticon’s extension will come in handy, as you’ll be able to access the largest database of free icons. Now that the prescription is complete, customize the presentation template and share your findings!
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Present your clinical case to the medical community with this dynamic and engaging presentation by Slidesgo. Who said science can't be creative and fun?
Free medical Google Slides themes and PowerPoint templates to present a concise, organized Clinical Case Report. Customize them with the easy-to-edit graphic resources included, and create an effective presentation.
Enhance medical presentations with our Case Presentation Templates. Streamline communication, enhance clarity, and deliver effective medical reports.
Explain your latest Clinical Case with this interactive and animated Google Slides theme and PowerPoint template. It's perfect for medical topics!
A clinical case study is a report where medical practitioners share a patient's case. Generally, clinical case studies are valuable tools for medical research as they provide detailed information on the development of a disease or illness in particular individuals. Use this PowerPoint template to document extraordinary patient cases and share your findings with the healthcare community. You ...
Clinical case reports have been the earliest form of medical communication. A clinical case report or case study is a means of disseminating new knowledge gained from clinical practice. Medical practitioners often come across patient cases that are different or unusual such as a previously unknown condition, a complication of a known disease, an unusual … Continue reading "Clinical Case"
This presentation template offers you the opportunity to present clinical cases to peers and attendings. You can also use it to present patient history and course of treatment during your oral board certification exam.
This PowerPoint template designed for clinical case studies provides a user-friendly platform for creating impactful presentations. It is ideal for medical professionals looking to enhance their educational sessions or research discussions. The template allows customization of slides to include patient details, diagnostic findings, treatment ...
The Medical Case Study PowerPoint Template is a 10-slide presentation providing a variety of infographic layouts. These slides include several presentation icons, and clip art PowerPoint shapes relevant to the healthcare industry. For example, the icon of heart rate graph, human heart, stethoscope, first aid, operation symbols, and health ...
A medical case study is an in-depth analysis of a patient's health condition, encompassing their medical history, symptoms, diagnosis, treatment, and outcomes, providing valuable insights for medical education and research. This comprehensive template is tailored to meet the specific needs of healthcare professionals, educators, and researchers.
Download the PowerPoint template or Google Slides theme Clinical Case 04-2019 free of charge. With this template you can create presentations educational. This theme includes the color blue.
This clinical case study template for PowerPoint and Google Slides stands out a lot for its eye-catching images and 100% editable tools. In its 36 slides you can find a background color scheme that is very pleasing to the human eye. In addition, you can make effective and quick presentations, very easily, just download this free ppt file and take it to Canva editing.
Free Google Slides theme, PowerPoint template, and Canva presentation template. Slidesgo is back with a new free medical template, perfect for a presentation about a clinical case. The design is very appealing, so these slides are a nice tool to provide a lot of useful information for doctors and researchers.
Here are the 7 parts of a patient case presentation template, plus some advice on how to practice your presentation skills. Learn more.
We've collected the top free PowerPoint case study presentation templates with or without sample text. Marketing and product managers, sales execs, and strategists can use them to arrange and present their success stories, strategies, and results.
Submitting a clinical report requires rigor and a detailed scheme. With the Clinical Case Report Free Presentation Helse you will have curated schemes and info to make your speech a success! Helse has slides dedicated to the case presentation, the discussion on the subject, existing literature and conclusion.
Designing an eyecatching presentation template is time-consuming. Download the following free and ready-to-use Clinical case powerpoint templates and Google slides themes for the upcoming presentation.
The case study PowerPoint templates can enhance your presentations by providing a professional and organized layout specifically designed for showcasing detailed research and analysis. With its visually appealing design and customizable features, it allows you to effectively present your case study findings and engage your audience.
Behavioral Health Case Presentation Template. DO NOT INCLUDE ANY PATIENT IDENTIFIERS. Please note that case consultations do not create or otherwise establish a provider-patient relationship between any Piedmont Health Services or UNC Health clinician. Presenter name: Juan Prandoni, PhD, HSP-PA, LPA. Presenter Clinical Role:
Get inspiration for Clinical Case Study Powerpoint Template. Browse through our huge selection of community templates or smoothly transition your PowerPoint into Prezi. Create engaging presentations and impress your audience with your visual story.
Free Google Slides theme, PowerPoint template, and Canva presentation template. Clinical cases are very important and serve as a good source of reliable information, since they present a detailed report of things such as symptoms, diagnosis and treatment of a patient. This new free medical template by Slidesgo will help you with the hard task ...
should select a clinical case that is the same as the one they present in their oral Clinical Case Presentation (see page 21, below), but they are free to select a different case if they want to do so. The case study will follow the format used in the journal Clinical Case Studies with the addition of sections on ethics and diversity.
Case example of a prospective use of the LANS criteria in clinical settings. This patient was seen at Mayo Clinic, Rochester, to determine eligibility for an anti-amyloid monoclonal antibody therapy, and the LANS criteria were internally defined at the time of evaluation.
Treating psychological and psychiatric conditions is quite important, as they affect our health to a large stent. To learn more about them, use this Mental Health Clinical Case presentation and give some info about case reports, using diagrams, tables, maps… Provide details about the patient, diagnosis, treatment or even the diagnosis.
Premium Google Slides theme, PowerPoint template, and Canva presentation template. When trying to prevent diseases, information is key, and if it's reliable, all the better. With this new free medical template, you can show the results of a clinical case, including the symptoms, the patient monitoring, the treatment and all the important data.