Creutzfeldt-Jakob disease in a post-COVID-19 patient: did SARS-CoV-2 accelerate the neurodegeneration?

Background: Creutzfeldt-Jakob disease (CJD) is a rare, fatal neurodegenerative disorder, with few months as a usual duration from onset to death. Case presentation: In this case report, a patient of Sporadic CJD (sCJD) who presented one month after severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. The diagnosis of this case was established after confirming findings from clinical, neurophysiology, radiological, and laboratory features of this disease. Conclusion: Putting in mind all the updated data on the pathogenesis of CJD and the immune responses to SARS-CoV-2, we can suggest that COVID-19 can lead to accelerated pathogenesis and exaggerated manifestations of this fatal neurodegenerative disease.

Creutzfeldt-Jakob Disease in a Patient with Previous COVID-19 Infection: "The Virus Caused the Derangement in My Brain".

Recent studies have speculated a link between Creutzfeldt-Jakob disease (CJD) and COVID-19, following the description of CJD cases after COVID-19 infection. We report the case of a 71-year-old female patient who developed neuropsychiatric and neurological symptoms after COVID-19 infection and was later diagnosed with CJD. Cerebrospinal fluid (CSF) total tau levels were slightly increased. She resulted prion protein gene (PRNP) M129V heterozygous. We aim to emphasize the role of the polymorphism at codon 129 of PRNP gene on the clinical phenotype and duration of CJD, and the CSF total tau levels that likely correlate with the rate of disease progression.

Application of real-time quaking-induced conversion in Creutzfeldt-Jakob disease surveillance.

BACKGROUND: Evaluation of the application of CSF real-time quaking-induced conversion in Creutzfeldt-Jakob disease surveillance to investigate test accuracy, influencing factors, and associations with disease incidence. METHODS: In a prospective surveillance study, CSF real-time quaking-induced conversion was performed in patients with clinical suspicion of prion disease (2014-2022). Clinically or histochemically characterized patients with sporadic Creutzfeldt-Jakob disease (n = 888) and patients with final diagnosis of non-prion disease (n = 371) were included for accuracy and association studies. RESULTS: The overall test sensitivity for sporadic Creutzfeldt-Jakob disease was 90% and the specificity 99%. Lower sensitivity was associated with early disease stage (p = 0.029) and longer survival (p < 0.001). The frequency of false positives was significantly higher in patients with inflammatory CNS diseases (3.7%) than in other diagnoses (0.4%, p = 0.027). The incidence increased from 1.7 per million person-years (2006-2017) to 2.0 after the test was added to diagnostic the criteria (2018-2021). CONCLUSION: We validated high diagnostic accuracy of CSF real-time quaking-induced conversion but identified inflammatory brain disease as a potential source of (rare) false-positive results, indicating thorough consideration of this condition in the differential diagnosis of Creutzfeldt-Jakob disease. The surveillance improved after amendment of the diagnostic criteria, whereas the incidence showed no suggestive alterations during the COVID-19 pandemic.

147th Annual Meeting American Neurological Association

The proceedings contain 417 papers. The topics discussed include: APOE is independently associated with the heterogeneity of cognitive decline rate in the normal aging-early Alzheimer's disease continuum;bioequivalence and safety comparison of once-weekly donepezil transdermal system with once-daily oral donepezil: results of a phase 1 trial in healthy volunteers;bleed type as a predictor of emotional and behavioral dyscontrol following intracerebral and subarachnoid hemorrhage;case series of manic symptoms following concussion;cognitive impairment in pulmonary hypertension;Creutzfeldt Jacob disease misdiagnosis, a diagnostic challenge and psychological burden: a case series;depressed neurocognitive function with comprehensive neuropsychiatric evaluation among long-haul COVID patients;evaluation of skin adhesion and local skin tolerability of once-weekly donepezil transdermal system: results of a phase 1 trial in healthy volunteers;determining etiologic diagnoses in rapidly progressive dementia: a clinical study;and frequency and distribution of transactive response DNA-binding protein 43 (TDP-43) pathology across the age spectrum in an elderly cohort with and without dementia.

Creutzfeldt-Jakob disease with neuroleptic malignant syndrome.

Creutzfeldt­Jakob disease (CJD) is a rare rapidly progressive fatal neurodegenerative disease. Neuroleptic malignant syndrome (NMS) is a complication of antipsychotic medications which may be used to treat neuropsychiatric symptoms of CJD. We present a case of a 51­year­ old woman with CJD who developed NMS after being prescribed quetiapine.

Creutzfeldt-Jakob disease: A case report and differential diagnoses.

Although sporadic Creutzfeldt-Jakob disease is a rare neurodegenerative disease and often difficult to diagnose at the earliest onset, meticulous clinical examination, electroencephalography, and neuroimaging findings will help in diagnosis.

SARS-CoV-2 Invasion and Pathological Links to Prion Disease.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the COVID-19 disease, is a highly infectious and transmissible viral pathogen that continues to impact human health globally. Nearly ~600 million people have been infected with SARS-CoV-2, and about half exhibit some degree of continuing health complication, generically referred to as long COVID. Lingering and often serious neurological problems for patients in the post-COVID-19 recovery period include brain fog, behavioral changes, confusion, delirium, deficits in intellect, cognition and memory issues, loss of balance and coordination, problems with vision, visual processing and hallucinations, encephalopathy, encephalitis, neurovascular or cerebrovascular insufficiency, and/or impaired consciousness. Depending upon the patient's age at the onset of COVID-19 and other factors, up to ~35% of all elderly COVID-19 patients develop a mild-to-severe encephalopathy due to complications arising from a SARS-CoV-2-induced cytokine storm and a surge in cytokine-mediated pro-inflammatory and immune signaling. In fact, this cytokine storm syndrome:&nbsp;(i) appears to predispose aged COVID-19 patients to the development of other neurological complications, especially those who have experienced a more serious grade of COVID-19 infection; (ii) lies along highly interactive and pathological pathways involving SARS-CoV-2 infection that promotes the parallel development and/or intensification of progressive and often lethal neurological conditions, and (iii) is strongly associated with the symptomology, onset, and development of human prion disease (PrD) and other insidious and incurable neurological syndromes. This commentary paper will evaluate some recent peer-reviewed studies in this intriguing area of human SARS-CoV-2-associated neuropathology and will assess how chronic, viral-mediated changes to the brain and CNS contribute to cognitive decline in PrD and other progressive, age-related neurodegenerative disorders.

A CLASSIC CASE OF CREUTZFELDT-JAKOB DISEASE (CJD)

CASE: A 64-year-old woman was brought in by husband for inability to care for patient. Previously active, she developed gait instability, slurred speech, and memory lapse to the point of selective mutism and being bed-bound within three months. Her medical history was notable for hypertension and Covid four months prior. She had had mild upper respiratory symptoms and recovered in ten days. Examination revealed general encephalopathy, dysarthria, limited ability to follow commands. She had decreased strength but increased tone and rigidity in all extremities. She had rhythmic jaw movement and bradykinesia with scatter myoclonic movements. Cerebellar exam was notable for ataxia, but she had normal cranial nerve and sensory exams and normal reflexes. MRI of the brain revealed restricted diffusion and T2/Flair signal abnormality involving bilateral basal ganglia, ventral medial thalami, hippocampi, and cerebral cortices. Toxic metabolic workup was unrevealing. CSF was positive for 14-3-3 protein and elevated total tau protein, confirming Creutzfeldt-Jakob disease. IMPACT/DISCUSSION: Creutzfeldt-Jakob Disease (CJD) is a prion disease with one in a million prevalence. Patients present with rapidly progressing dementia, myoclonus, and signs of cerebellar, corticospinal and extrapyramidal involvement including nystagmus, ataxia, hyperreflexia, spasticity, hypokinesia, bradykinesia, dystonia, and rigidity. CJD is fatal within months to two years. Patients with end stage disease may have akinetic mutism. Magnetic resonance imaging (MRI), electroencephalogram (EEG), and cerebrospinal fluid (CSF) analysis are important for evaluation of CJD. Most sensitive in early stages, MRI Brain commonly shows hyperintense signal involving the cerebral cortex, corpus striatum, caudate, and putamen. EEG may capture pattern of periodic bi-or triphasic period sharp wave complexes. CSF might detect 14-3-3 protein with elevation of tau protein but real-time quaking-induced conversion (RT-QuIC) has the highest specificity for diagnosis for CJD. Though brain biopsy is the sole method of definitive diagnosis, results of MRI, EEG, and CSF analysis along with presenting signs and symptoms are sufficient for clinical diagnosis of CJD. Our patient's dementia, myoclonus, ataxia, hypokinesia, bradykinesia, dystonia, and rigidity all progressing to akinetic mutism within three months are classic presentation of CJD. EEG was normal, but MRI with hyperintensity of basal ganglia and cerebral cortices and CSF analysis with positive 14-3-3 and elevated tau proteins are all lead to diagnosis of CJD. CONCLUSION: This case illustrates a classic case of a Creutzfeldt-Jakob Disease, a rare prion disease marked by rapidly progressive dementia with neuropsychiatric features.

Creutzfeldt-Jakob disease surveillance in Australia: update to 31 December 2021.

Nationwide surveillance of Creutzfeldt-Jakob disease (CJD) and other human prion diseases is performed by the Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR). National surveillance encompasses the period since 1 January 1970, with prospective surveillance occurring from 1 October 1993. Over this prospective surveillance period, considerable developments have occurred in pre-mortem diagnostics; in the delineation of new disease subtypes; and in a heightened awareness of prion diseases in healthcare settings. Surveillance practices of the ANCJDR have evolved and adapted accordingly. This report summarises the activities of the ANCJDR during 2021. Since the ANCJDR began offering diagnostic cerebrospinal fluid (CSF) 14-3-3 protein testing in Australia in September 1997, the annual number of referrals has steadily increased. In 2021, a total of 548 domestic CSF specimens were referred for 14-3-3 protein testing; 73 persons with suspected human prion disease were formally added to the national register. As of 31 December 2021, just over half of the 73 suspect case notifications (37/73) remain classified as 'incomplete'; 17 cases were classified as 'definite' and 13 as 'probable' prion disease; six cases were excluded through either detailed clinical follow-up (two cases) or neuropathological examination (four cases). For 2021, sixty-four percent of all suspected human-prion-disease-related deaths in Australia underwent neuropathological examination. No cases of variant or iatrogenic CJD were identified. The SARS-CoV-2 pandemic did not affect prion disease surveillance outcomes in Australia.

Two Probable Creutzfeldt-Jakob Disease Cases Within One Month in a Single Hospital inGrand Rapids, Michigan

Objective: NA Background: Creutzfeldt-Jakob disease (CJD) is an extremely rare but fatal neurodegenerative disease with incidence of one in a million worldwide, and few than 1000 cases per year in the United States per year. Design/Methods: NA Case Summary: We present two probable CJD cases seen in the same hospital within one month. Case one was a 67-year-old white female, former psychology practice manager, presenting with worsening cognition, vertigo, behavioral changes and 15 lb weight loss over 6 months. Exam findings significant for MoCA of 17/30 (decreased to 15/30 after one week), constant right eye shut, mild dysmetria in both lower extremities, a wide based gait with small strides. Blood work and initial Spinal fluid studies were negative. Continuous EEG showing occasional right temporal slow, frequent generalized rhythmic theta and delta slowing. MRI brain findings were suggestive of CJD with hyperintensities in bilateral caudate nucleus and putamen. Patient did not respond to high dose steroid. Case two was a 78-year-old white male, admitted for deterioration in cognition, gait, speech, fatigue and intermittent body jerking. Progression of his symptoms was so rapid, from a highly functional retired funeral director, he became minimal speech, loss of ADL within 3 months. Exam was significant for orientation to self only, global aphasia, muscle weakness and startle myoclonus. Blood work and initial spinal fluid studies were negative. MRI brain showed asymmetric cortically based diffuse restriction within cingulate, caudate nucleus also left temporoparietal. EEG showed generalized rhythmic delta activity. CSF from both cases eventually showed positive RT-QuIC, 14-3-3 protein and highly elevated T-Tau protein. Conclusions: CJD is a transmittable, reportable disease. Two cases seen in the same hospital within one month skews from the previously known CJD prevalence. Surveillance and investigation on the reason of regional CJD arise during COVID-19 pandemic may prove to be important and urgent.

CREUTZFELDT-JAKOB DISEASE: ACCELERATED BY COVID?

TYPE: Late Breaking TOPIC: Chest Infections INTRODUCTION: Creutzfeld Jakob Disease (CJD) is a collective group of rare neurodegenerative diseases characterized by rapidly progressing cognitive decline, deficits in cortical function (aphasia, apraxia, agnosia), myoclonic jerks and extrapyramidal symptoms with a mortality of 100%. CASE PRESENTATION: We present a 72-year-old female who initially presented with aphasia, dyscalculia, right hemiparesis and dysgraphia.Upon arrival, she was hemodynamically stable and labs were remarkable for a positive COVID PCR test. CT head and CT angiogram was within normal limits. MRI was nonspecific. EEG showed left temporal lateralized periodic discharges (PLDs) at 1 Hz with a triphasic morphology and Lumbar puncture disclosed a protein of 79 mg/dL, glucose 65 mg/dL, WBC 1, HSV 1 and 2 PCR, cryptococcus, gram stain/culture AFB, and cytology were all negative. With concern for autoimmune encephalitis she was empirically started on IVIG without improvement. Paraneoplastic and autoimmune evaluation resulted pan negative. 14-3-3 CSF protein assay reported positive and diagnosis CJD was made. After goals of care discussion with the family, she was discharged home with hospice. DISCUSSION: Sporadic type (sCJD) accounts for about 85% of cases and occurs after somatic mutation in the gene for PrP protein. Rapid neurocognitive decline and cortical function deficits with negative infectious, autoimmune, and paraneoplastic workups should prompt further evaluation for CJD. CSF protein 14-3-3 has a sensitivity of 92%–96% for sCJD. EEG showing of a 1/second periodic triphasic sharp wave complex is present in 1/3 cases. CONCLUSIONS: Most recently, there have been some case reports indicating that the systemic immune response in COVID-19 could accelerate the clinical course of sCJD, however, a potential causal link remains unclear. DISCLOSURE: No significant relationships. KEYWORD: CJD

Creutzfeldt-Jakob disease after COVID-19: infection-induced prion protein misfolding? A case report.

Creutzfeldt-Jakob disease (CJD) is a rare, fatal disease presenting with rapidly progressive neurological deficits caused by the accumulation of a misfolded form (PrPSc) of prion protein (PrPc). Coronavirus disease 2019 (COVID-19) is a primarily respiratory syndrome caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); many diverse neurological complications have been observed after COVID-19. We describe a young patient developing CJD two months after mild COVID-19. Presenting symptoms were visuospatial deficits and ataxia, evolving into a bedridden state with preserved consciousness and diffuse myoclonus. Diagnostic work-up was suggestive of CJD. The early age of onset and the short interval between respiratory and neurological symptoms might suggest a causal relationship: a COVID-19-related neuroinflammatory state may have induced the misfolding and subsequent aggregation of PrPSc. The present case emphasizes the link between neuroinflammation and protein misfolding. Further studies are needed to establish the role of SARS-CoV-2 as an initiator of neurodegeneration.

A Case of Hashimoto's Encephalopathy Presenting with Cognitive Impairment and Visual Hallucinations

Introduction: Hashimoto's encephalopathy (HE) is a rare immune–mediated complication of Hashimoto thyroiditis. It is presented as subacute onset of altered mental status with confusion, seizures and myoclonus. It is a diagnosis of exclusion and requires that all other possible causes of cognitive impairment are excluded with a response to steroid therapy and evidence of thyroid autoimmunity in a patient. Here, we present a case of HE in a patient who presented with altered mental status and visual hallucinations despite no history or symptoms of thyroid disorder. Case Description: A 77 year old male with past medical history of hypertension presented with altered mental status, lethargy, and visual hallucinations. Per patient’s wife, patient started to get somnolent and was having memory problems six weeks prior to presentation. His mental status gradually deteriorated, and he started to have visual hallucinations. He was somnolent and noted to have myoclonus and twitching on admission. Magnetic resonance imaging (MRI) of the brain with gadolinium showed chronic microvascular changes with no acute intracranial pathology or masses. Electroencephalogram (EEG) showed no signs of epileptiform activity. Infectious disease work up, including complete blood count, urinalysis, sexually transmitted diseases, and cerebrospinal fluid (CSF) analysis, was negative. Blood glucose levels, serum electrolytes, liver function tests, blood urea nitrogen, and creatinine were normal. Coronavirus disease 2019 (COVID-19) was negative. CSF analysis for autoimmune encephalopathy and Creutzfeldt-Jakob disease was negative. Thyroid function tests were normal. Thyroid peroxidase antibody (TPOAb) was negative (8.6 IU/mL [reference range (RR): < 9.0 IU/mL]) and TgAb was positive (8.2 ng/ mL [RR: < 4 IU/ mL]). With suspicion of Hashimoto's encephalopathy, he was started on intravenous Solu-Medrol 1 g for five days. He was then switched to oral prednisone 60 mg daily, which he received for ten days. His mental status improved upon day 14 of admission. On day 17 of admission, he was discharged on oral prednisone 40 mg daily with taper for five weeks. He was evaluated in the clinic few months after discharge. His mental status had improved significantly, and he was back to his baseline in about two months after discharge as per his wife. Repeat thyroid function tests, TPOAb, and TgAb were negative. Discussion: The incidence of Hashimoto’s encephalopathy (HE) is 2.1 per 100,000 individuals in the general population, and is more common in women than men. This case highlights that HE should be considered in patients with subacute presentation of neurological problems, which cannot be explained with other possible diagnosis, despite no symptoms of thyroid disease such as the patient in this case study. Therefore, HE should be evaluated for in patients with cognitive impairment for prompt diagnosis and treatment with steroid therapy in order to improve the prognosis in these patients.

Characteristics of Creutzfeldt-Jakob disease cases reported by surveillance network in China, 2020

Objective: To investigate the incidence, epidemiology and clinical characteristics of Creutzfeldt-Jakob disease (CJD) in China in 2020.

Creutzfeldt-Jakob Disease After the Coronavirus Disease-2019 Vaccination

Reports of neurological problems are increasing for the clinical presentation of coronavirus disease-2019 (COVID-19). The clinical presentation reported in this study seemed to be a combination of nonspecific complications of the systemic disease, inflammation of the cerebrovascular system, and the effects of a direct viral infection. Creutzfeldt-Jakob disease, a spongiform encephalopathy caused by prions, is characterized by a severe neurological destruction, which has an extremely high mortality. In this publication, we presented a patient who was admitted to the Pamukkale University Anesthesiology Intensive Care Units with the neurological findings that developed after the COVID-19 vaccine (CoronaVac, Sinovac Life Sciences, Beijing, China). The patient died due to the progressive neurological disorders. In cases where rapidly progressive neurological disorders are observed, Creutzfeldt-Jakob disease should be considered and the role of immunity-related conditions in the progression of the disease should be investigated. (English) [ FROM AUTHOR] Koronavirüs hastalığı-2019 (COVID-19) hastalığının klinik seyrinde gelişen nörolojik problemlerle ilgili raporlar artmaktadır. Bu klinik tablo, sistemik hastalığın spesifik olmayan komplikasyonları, serebrovasküler sistem iltihabı veya doğrudan viral enfeksiyonun etkilerinin bir kombinasyonu gibi görünmektedir. Prionların neden olduğu süngerimsi bir ensefalopati olan Creutzfeldt-Jakob hastalığı, şiddetli nörolojik yıkım ile karakterizedir ve son derece yüksek bir ölüm oranına sahiptir. Bu yayında, Pamukkale Üniversitesi Anesteziyoloji Yoğun Bakım Ünitesi’ne COVID-19 aşısı (CoronaVac, Sinovac Life Sciences, Beijing, China) sonrası gelişen nörolojik bulgularla başvuran bir hastayı sunduk. Hasta ilerleyici nörolojik bozukluklar nedeniyle öldü. Hızla ilerleyen nörolojik bozuklukların görüldüğü durumlarda Creutzfeldt-Jakob hastalığı düşünülmeli ve bağışıklıkla ilgili durumların hastalığın ilerlemesindeki rolü araştırılmalıdır. (Turkish) [ FROM AUTHOR] Copyright of Turkish Journal of Intensive Care is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

Case Report: Neurodegenerative Diseases After Severe Acute Respiratory Syndrome Coronavirus 2 Infection, a Report of Three Cases: Creutzfeldt-Jakob Disease, Rapidly Progressive Alzheimer's Disease, and Frontotemporal Dementia.

The relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and neurodegenerative diseases is yet to be fully clarified. Rapid worsening and even new-onset cases of those disorders have been reported in association with coronavirus disease 2019 (COVID-19). We describe three cases of neurodegenerative diseases in patients with SARS-CoV-2: a case of Creutzfeldt-Jakob disease during the COVID-19 acute phase, to our knowledge, is the second one described in the literature; a rapidly progressive Alzheimer's Disease; and a patient with frontotemporal dementia, and a quick decline of both cognitive and behavioral domains. This report suggests an association between SARS-CoV-2 infection and a higher probability of developing or accelerating neurodegenerative chronic neurologic conditions. We reinforce the need for a close cognitive follow-up in the aftermath of Sars-Cov2 infection.

COVID-19-associated encephalitis or Creutzfeldt-Jakob disease: a case report.

Background: Accurate diagnosis and management of patients with rapidly progressive dementia may be challenging during the COVID-19 pandemic, which has negatively influenced the diagnostic performances, medical resource allocation and routine care for all non-COVID-19 diseases. Case presentation: We herein present a case of a 57-year-old male with rapidly progressive cognitive decline, headache, diplopia, myalgia, unsteady gait, aggression, depression, insomnia, hallucinations and delusions of persecution. COVID-19-associated encephalitis was briefly considered as a differential diagnosis. However, this hypothesis was rejected upon further investigation. A final diagnosis of sporadic Creutzfeldt-Jakob disease was made. Conclusion: A timely and accurate diagnosis of Creutzfeldt-Jakob disease gives patients and their families the chance to receive a good standard of healthcare and avoid extensive evaluations for other conditions.

Clinical and Radiological Deterioration in a Case of Creutzfeldt-Jakob Disease following SARS-CoV-2 Infection: Hints to Accelerated Age-Dependent Neurodegeneration.

Systemic inflammation and the host immune responses associated with certain viral infections may accelerate the rate of neurodegeneration in patients with Creutzfeldt-Jakob disease (CJD), a rare, transmissible neurodegenerative disease. However, the effects of the newly emerged SARS-CoV-2 infection on the pathogenesis of CJD are unknown. In this study, we describe the case of an elderly female patient with sporadic CJD that exhibited clinical deterioration with the emergence of seizures and radiological neurodegenerative progression following an infection with SARS-CoV-2 and severe COVID-19. Despite efforts to control the progression of the disease, a dismal outcome ensued. This report further evidences the age-dependent neurological effects of SARS-CoV-2 infection and proposes a vulnerability to CJD and increased CJD progression following COVID-19.

Human Prion Disorders: Review of the Current Literature and a Twenty-Year Experience of the National Surveillance Center in the Czech Republic.

Human prion disorders (transmissible spongiform encephalopathies, TSEs) are unique, progressive, and fatal neurodegenerative diseases caused by aggregation of misfolded prion protein in neuronal tissue. Due to the potential transmission, human TSEs are under active surveillance in a majority of countries; in the Czech Republic data are centralized at the National surveillance center (NRL) which has a clinical and a neuropathological subdivision. The aim of our article is to review current knowledge about human TSEs and summarize the experience of active surveillance of human prion diseases in the Czech Republic during the last 20 years. Possible or probable TSEs undergo a mandatory autopsy using a standardized protocol. From 2001 to 2020, 305 cases of sporadic and genetic TSEs including 8 rare cases of Gerstmann-Sträussler-Scheinker syndrome (GSS) were confirmed. Additionally, in the Czech Republic, brain samples from all corneal donors have been tested by the NRL immunology laboratory to increase the safety of corneal transplants since January 2007. All tested 6590 corneal donor brain tissue samples were negative for prion protein deposits. Moreover, the routine use of diagnostic criteria including biomarkers are robust enough, and not even the COVID-19 pandemic has negatively impacted TSEs surveillance in the Czech Republic.

Impact of COVID-19 Pandemic on Patients With Neurodegenerative Diseases.

COVID-19 pandemic has already produced great impacts on global health security and social-economy. Elderly, particularly those with underlying diseases, are suffering from higher fatality rate. Neurodegenerative diseases are a group of incurable neurological disorders of loss of neuron and/or myelin sheath, which affect hundreds of millions of elderly populations and usually need long-term care. Older population is one of the most vulnerable to COVID-19 pandemic. In this report, we reviewed the current status of COVID-19 on the patients with several neurodegenerative diseases, particularly Alzheimer's disease, Parkinson's disease, prion disease, and amyotrophic lateral sclerosis. Meanwhile, the potential mechanisms of SARS-CoV-2 infection in the pathogenesis of neurodegenerative diseases were also summarized.