Case Report Open Access
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Apr 26, 2024; 12(12): 2065-2073
Published online Apr 26, 2024. doi: 10.12998/wjcc.v12.i12.2065
Human immunodeficiency virus-associated dementia complex with positive 14-3-3 protein in cerebrospinal fluid: A case report
Yun-Sen He, Department of Neurosurgery, Sichuan Lansheng Brain Hospital & Shanghai Lansheng Brain Hospital Investment Co., Ltd., Chengdu 610036, Sichuan Province, China
Xiao-Hong Qin, Meng-Jun Zhang, Department of Psychiatry, Sichuan Provincial Center for Mental Health, Chengdu 610072, Sichuan Province, China
Min Feng, Department of Geriatrics, Municipal People’s Hospital in Luzhou, Luzhou 646000, Sichuan Province, China
Qin-Jiang Huang, Department of Neurosurgery, Wenjiang District People’s Hospital of Chengdu, Chengdu 611100, Sichuan Province, China
Li-Li Guo, Ming-Bin Bao, Ye Tao, Bo Wu, Department of Neurosurgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China Chengdu, Chengdu 610072, Sichuan Province, China
Hong-Yuan Dai, Department of Neurology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu 610072, Sichuan Province, China
ORCID number: Hong-Yuan Dai (0000-0002-7249-4113); Bo Wu (0000-0003-3448-267X).
Co-first authors: Yun-Sen He and Xiao-Hong Qin.
Co-corresponding authors: Hong-Yuan Dai and Bo Wu.
Author contributions: Min F contributed to investigation, writing – original draft, review and editing; Huang QJ, Zhang MJ, Bao MB, Tao Y, Wu B, and Dai HY contributed to writing – review and editing; He YS, Qin XH, Min F, Huang QJ, Zhang MJ, Bao MB, Tao Y, and Wu B contributed to data curation; He YS, Qin XH, Min F, and Wu B contributed to methodology; He YS, Qin XH, Huang QJ, Zhang MJ, Bao MB, Tao Y, and Dai HY contributed to the resources; Tao Y contributed to funding acquisition; Dai HY contributed to conceptualization. He YS and Qin XH contributed equally to writing the original draft and to formal analysis, and merit co-first authorship. Dai HY and Wu B have each made distinct contributions to this case report, encompassing clinical treatment and the writing of the case report, respectively, and merit co-corresponding authorship; Dai HY was involved in the clinical treatment and the extended follow-up of this case, as well as verifying the authenticity of clinical data and patient outpatient consultations; Wu B participated in the search for relevant literature, guided the writing of this case report, and was involved in editing, proofreading, and submitting the manuscript. All authors have read and approved the final manuscript.
Informed consent statement: Informed written consent was obtained from the patient for publication of this report.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Corresponding author: Hong-Yuan Dai, MD, Chief Physician, Doctor, Department of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32 West Section 2, First Ring Road, Chengdu 610072, Sichuan Province, China.
Received: October 28, 2023
Peer-review started: October 28, 2023
First decision: December 12, 2023
Revised: December 22, 2023
Accepted: March 14, 2024
Article in press: March 14, 2024
Published online: April 26, 2024


Human immunodeficiency virus (HIV)-associated dementia (HAD) is a subcortical form of dementia characterized by memory deficits and psychomotor slowing. However, HAD often presents with symptoms similar to those of Creutzfeldt-Jakob disease (CJD), particularly in patients with acquired immune deficiency syndrome (AIDS).


We report the case of a 54-year-old male who exhibited cognitive dysfunction and secondary behavioral changes following HIV infection and suspected prion exposure. The patient was diagnosed with HIV during hospitalization and his cerebrospinal fluid tested positive for 14-3-3 proteins. His electroencephalogram showed a borderline-abnormal periodic triphasic wave pattern. Contrast-enhanced magnetic resonance imaging revealed moderate encephalatrophy and demyelination. Initially, symptomatic treatment and administration of amantadine were pursued for presumed CJD, but the patient’s condition continued to deteriorate. By contrast, the patient’s condition improved following anti-HIV therapy. This individual is also the only patient with this prognosis to have survived over 4 years. Thus, the diagnosis was revised to HAD.


In the diagnostic process of rapidly progressive dementia, it is crucial to rule out as many potential causes as possible and to consider an autopsy to diminish diagnostic uncertainty. The 14-3-3 protein should not be regarded as the definitive marker for CJD. Comprehensive laboratory screening for infectious diseases is essential to enhance diagnostic precision, especially in AIDS patients with potential CJD. Ultimately, a trial of diagnostic treatment may be considered when additional testing is not feasible.

Key Words: HIV-associated dementia, Cognitive dysfunction, Creutzfeld-Jakob disease, Rapidly progressive dementia, Case report

Core Tip: In the present case report, we excluded an extremely rare patient with human immunodeficiency virus (HIV) and cerebrospinal fluid 14-3-3 protein-positive. Unlike the previously reported 7 cases, our patient had sustained improvement with anti-HIV therapy and was also the only patient in this entity to survive. Consequently, our report provided a completely different reference for managing rapidly progressive dementia in particular cases.


Human immunodeficiency virus (HIV)-associated dementia (HAD) is subcortical dementia characterized by memory deficits and psychomotor slowing, which occurs after the brain is infected with the HIV[1]. Cognitive dysfunction is a common symptom in patients with acquired immune deficiency syndrome (AIDS) and non-opportunistic infections caused by other viruses. Creutzfeldt-Jakob disease (CJD), also known as Cortico-striatum-myeloid degenerative disease, is characterized by mental disorders, dementia, Parkinson-like manifestations, ataxia, myoclonus, and muscle atrophy. CJD is a chronic and progressive disease caused by a rare infection with the prion protein[2]. Additionally, the cerebrospinal fluid (CSF) 14-3-3 protein is an essential marker for diagnosing CJD.

Here, a rare case is presented of a patient with AIDS and a positive 14-3-3 protein[2]. Although similar cases have been reported[3-7], this case provides new insights and is an important learning point for managing patients with rapidly progressive dementia due to its distinct diagnosis, treatment, and efficacy.

Chief complaints

A 54-year-old male (Han ethnicity) presented to the neurology clinic of our institution with a 6 mo history of slurred speech that had worsened over the past 3 months.

History of present illness

The patient had suffered from memory disturbances for more than 1 year, with symptoms primarily including progressive memory loss and episodic anterograde amnesia. Additionally, he had developed an unstable gait. Initially diagnosed with brain atrophy, his symptoms had intensified after treatment at another facility, from which no case report was provided. One year prior, the patient had exhibited unclear speech, pain at the base of the tongue, and general malaise.

Additionally, dizziness, and left ear tinnitus were occasionally noted but he did not present physical signs of dysphagia or choking. The patient rejected therapy until 3 months ago when the above conditions were aggravated and the patient became unable to take care of himself. During the first consultation in our clinic on July 13, 2018, the patient demonstrated advanced manifestations of unsteady gait with one reported fall (details unavailable); severe cognitive dysfunction; hypopsychosis, which gradually became silent; and significantly decreased speech. Functionally, the patient was unemployed and lost self-care ability.

History of past illness

The patient’s past medical history was unremarkable.

Personal and family history

The patient had no history of exposure to toxic substances or family history of specific genetic diseases.

Physical examination

The patient was alert and entered the ward with a normal gait. He exhibited slurred speech, uncontrolled frowning, and pursing of the lips. Neurological deficits were noted, including impairments in memory, orientation, reasoning, and emotional expression. Meningeal signs were absent. The pharyngeal reflex was diminished, limb muscle tone was heightened, the Babinski sign was positive, and there was evident dysmetria on the finger-to-nose test (more pronounced on the left side) and the heel-to-knee test. Additionally, the patient tested positive for the Romberg sign, but there were no signs of tongue deviation or other pathological indicators.

Laboratory testing

Upon his admission, the family reported abnormality on the Mini-Mental State Examination and Montreal Cognitive Assessment tests during a previous assessment at another hospital, although the medical records from that visit were not available to us. Following his admission, an initial HIV antibody screening returned positive results, prompting us to perform a confirmatory HIV antibody test on the patient’s blood (the final results were pending at that time). Laboratory tests indicated leukocytopenia with a white blood cell count of 3.2 × 109/L and lymphocytes at 0.96 × 109/L. Analysis of T cell subsets showed a T helper (TH)/T suppressor (TS) ratio of 0.1, with TH/inducer (cluster of differentiation 4 [CD4]) cells at 78/µL and TS/killer (CD8) cells at 1218/µL. In addition, the patient’s CSF protein concentration was elevated at 0.73 g/L. The CSF cell count was normal, and extensive CSF testing for biochemical markers, routine cultures (including bacteria, fungi, Mycobacterium tuberculosis, and Cryptococcus), and antibodies associated with autoimmune and paraneoplastic encephalitis all returned negative results. Liver and kidney functions were normal, as were tests for anti-thyroid peroxidase antibody, anti-thyroglobulin antibody, ceruloplasmin, anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, folic acid, and vitamin B12 levels. The CSF tested positive for the 14-3-3 protein, and genotyping confirmed 129 M/M and 219 E/E variants (Figure 1). An electroencephalogram (EEG) showed borderline abnormalities with periodic triphasic waves, which were not indicative of a typical disorder.

Figure 1
Figure 1 The 14–3–3 protein was found in cerebrospinal fluid, and 129 M/M and 219 E/E genotype was further verified. The 14-3-3 protein was positive, and the protein gene test showed M/M type.
Imaging examination

Cranial computed tomography (CT) revealed cerebral atrophy and demyelination abnormalities in the white matter (Figure 2), given the multiple pinpoint hypodensities within the white matter exhibited in the bilateral basal ganglia with non-enhancement in all lesions and was initially diagnosed with lacunar infarction (Figure 2A). Medium encephalatrophy imaging accompanying white matter demyelination around the bilateral cerebral ventricle on T2-weighted images with pre-contrast c-magnetic resonance imaging (MRI) (Figure 2B). Meanwhile, 3–5 punctate hypodense lesions were identified in the bilateral basal ganglia on post-contrast MRI scans, with no evidence of enhancement (Figure 2C). Furthermore, the diffusion-weighted imaging (DWI) sequences on MRI did not display the characteristic “satin-like” high signal (Figure 2D).

Figure 2
Figure 2 Pre- and post-treatment cranial imaging examinations of the patient. A-D: Neuroradiological presentation of this patient before treatment; The brain computed tomography reveals encephalatrophy and demyelination in the white matter (A); Axial T1-weighted brain magnetic resonance imaging (MRI) with pre-contrast shows mild encephalatrophy and demyelination around the bilateral cerebral ventricles (B); Axial T1-weighted brain MRI with post-contrast displays no enhancement of any lesions (C and D); E and F: Neuroradiological presentation of this patient after treatment; Axial T1-weighted brain MRI with pre-contrast illustrates slight encephalatrophy and the significantly improved demyelination in the white matter around the bilateral cerebral ventricles (E); Axial T1-weighted brain MRI with post-contrast demonstrates no enhancement in any of the lesions (F).

HIV-associated dementia.


The patient's condition worsened while awaiting a conclusive AIDS diagnosis. We treated the patient with symptomatic treatment and amantadine (Amantadine Hydrochloride Tablets, USP) for CJD, which was the initial diagnosis considered. Despite these measures, the patient's health continued to decline. During this period, confirmatory tests for HIV antibodies returned positive results.

The patient was subsequently transferred to a specialized local center for infectious disease control to receive targeted treatment. Over the course of 4 years, the anti-HIV regimen provided by the center consisted of efavirenz (600 mg daily), tenofovir disoproxil (300 mg daily), lamivudine (100 mg daily), and compound sulfamethoxazole tablets (480 mg twice a day). The patient experienced rapid amelioration of symptoms following the commencement of antiretroviral therapy during his hospital stay.


Four years later, during a comprehensive outpatient follow-up assessment the patient exhibited clear consciousness and coherent speech; while recent memory and emotional expressiveness were mildly diminished, they were only marginally below the normal range; and the orientation and logical thinking functions were unremarkable. The limb muscle tension slightly increased, and the muscle strength was normal. The neurological signs and other symptoms were normal. The neuroradiological re-examination of the c-MRI (Figure 2E) revealed that the mild cerebral atrophy accompanying obvious demyelination in the white matter around the bilateral cerebral ventricle had improved than previous imaging. Additionally, several punctate hypointense lesions were spotted in the bilateral basal ganglia, exhibiting no enhancement (Figure 2F). The comparative scales and additional assessments conducted before and after treatment are summarized in Table 1.

Table 1 Comparison of conditions between before and after treatment with anti-human immunodeficiency virus.
Test items
Muscle strengthVV
Pathological reflex(-)(-)
Neuroradiology (+)Improvement

CJD is a degenerative central nervous system disease caused by prion proteins, mainly manifested as advancing dementia, myoclonus, cerebellar ataxia, and akinetic mutism[8]. The average survival from onset to death is only a few months[3-7]. According to its etiology, CJD is mainly divided into four types: Sporadic (accounting for approximately 85%), hereditary/family (5%-15%), iatrogenic, and variant (0%-10%)[2]. Sporadic (sCJD) hinges on rapidly progressive cognitive decline, verified through neuropathological examination or supportive immunochemical or biochemical markers. For a tentative diagnosis of sCJD, clinical symptoms must be corroborated by additional tests, such as an EEG showing periodic sharp wave complexes, DWI exhibiting the ribbon sign, elevated 14-3-3 protein levels in the CSF, and a positive real-time quaking-induced conversion (RT-QuIC) test[9].

In their comprehensive review of the literature from 1995 to 2011, Muayqil et al[10] analyzed 38 studies involving 1849 suspected cases of sCJD with 14-3-3 protein assays conducted. Their findings indicated that the 14-3-3 protein is a valuable diagnostic marker for sCJD with a sensitivity of 92% and specificity of 80%. Furthermore, the detection of prions through RT-QuIC has demonstrated enhanced diagnostic accuracy, boasting a sensitivity of 96% and specificity reaching 100%[11,12].

MRI sensitivity is 80% in CJD[9,11,13,14], Some studies put the sensitivity as high as 92% to 98%[15-17]. At the same time, its specificity is 74%–98%[9,13].

Periodic sharp-wave complexes (PSWCs) at a frequency of 1 Hz are a hallmark EEG pattern for CJD, demonstrating a sensitivity of 64% and a specificity of 91% in diagnosis[18]. The molecular classification of sporadic CJD hinges on polymorphisms at codon 129 (M and V) and the PrP^Sc glycotype (1 and 2), leading to distinct molecular subtypes such as MM1 and MV1[9]. Crucially, a single somatic mutation in the prion protein (PRNP) gene, specifically at M129V and E219K, is implicated in CJD pathogenesis[19]. The frequency of this gene mutation varies across ethnicities, with the Han population showing a higher propensity for the 129 M/M genotype, which correlates with an earlier disease onset. Notably, typical PSWCs generally manifest in the later stages of the disease and are less common in MV2, VV2, and MM2 subtypes[9].

In such cases, the diagnosis of probable CJD should meet the criteria for symptomatology, ancillary tests, and exclusion. Symptomatically: First: Rapidly progressive cognitive impairment. (1) Myoclonus; (2) Visual or cerebellar disturbance; (3) Pyramidal or extrapyramidal signs; and (4) Akinetic mutism. Ancillary criteria include: (1) Typical EEG; (2) Typical brain MRI; and (3) Positive CSF 14-3-3. Simultaneously, other possible diseases must also be excluded. Possible diagnostic criteria for CJD must meet the first and second symptoms (at least two), a positive criterion on a combined auxiliary test. Of course, other possible diseases must be ruled out to be diagnosed as probable CJD. A probable diagnosis of CJD is sufficient, in addition to meeting the criteria for the first and second symptoms (at least two), with a duration of less than 2 years. The PRNP test demonstrated M/M type, which increased the suspicion of CJD. Despite the strong consideration of HAD in this patient, the likelihood of probable CJD should still be taken into account during their hospital stay.

HAD is a common neurological complication after HIV infection and is mainly associated with memory impairment, motor coordination difficulties, cognitive deficits, difficulty performing complex tasks, and behavioral changes, including apathy and atypical reactions[1,20].

Most patients initially present with only short-term memory disorders in the early stages of AIDS; however, as the disease progresses, HIV-related chronic inflammation and immune activation may affect multiple brain regions. This can lead to dysfunctions in memory, cognition, language expression, and comprehension. With the widespread application of highly active antiretroviral therapy, the life expectancy of patients with HIV has significantly increased. Despite this, the incidence of moderate neurocognitive impairments remains high. A possible reason is that most anti-HIV drugs do not efficiently cross the blood-brain barrier to enter the central nervous system (CNS), resulting in insufficient drug concentrations in the CNS. Combined with the environmental factors within the CNS, HIV is prone to mutation, and the chronic accumulation of neurotoxicity leads to moderate neurocognitive dysfunction[20].

In this case, the diagnosis was considered infectious dementia combined with the medical history of the patient and auxiliary examination. The prime suspect was HIV, based on the following. Both HIV antibody screening test and HIV antibody confirmatory tests were positive. The apparent symptoms, including memory disorders, slowed mental processing, and behavioral disorders, were the primary symptoms of HAD, and there was a significant decrease in the patient's ability to perform daily activities. Regarding neuroradiology, CT and c-MRI revealed brain atrophy, demyelination, and white matter changes without enhancement. Consequently, the information above was consistent with HIV infection.

Four years after initiating anti-HIV treatment, we noted improved cognitive function and self-care abilities. However, memory remained worse than before; therefore, it is possible that prions may also play a role in the patient's rapid progressive dementia (RPD), Additionally, we speculate that HIV and CJD are not entirely coincidental as previously suggested[4,6].

Patients with co-infection of HIV and prions are very rare. To the best of our knowledge, only 5 cases have been diagnosed to date, and 3 others including our patient are highly suspected (Table 2). Unlike previously reported cases, our patient demonstrated sustained improvement following anti-HIV therapy and is the only known survivor. Our report provides a completely different reference for managing such cases.

Table 2 Difference between a previous case report about rapidly progressive dementia with human immunodeficiency virus and current report.
Babi et al[4]2016Male66United StatesConceptual apraxia, apathy, memory impairment, and gait disturbance, ataxia with gait disturbance, chronic peripheral neuropathyCSF: 14-3-3(+); T-Tau(+); RT-Qu IC(+); MRI: signal abnormalities in the bilateral caudate, putamen, and thalami, as well as gyriform cortical; EEG: (-); PRNP: N/A; Autopsy: CJDSporadic CJDPalliative carePassed away (3 months)
Eimer et al[7]2018Male59CaucasianMildly disoriented being insecure about the situation and locationCSF: 14-3-3(+); MRI: signal abnormalities in the caudate nuclei, frontal cortex, and parietal cortex bilaterally; EEG: periodic triphasic spike and wave complexes; PRNP: M129V; Autopsy: CJDSporadic CJDPalliative carePassed away (2 months)
Abu-Rumeileh et al[3]2018Male62ItalyDrowsy, with reduced verbal fluency, miotic reagent pupils, and a mask face. Axial and limb plastic hypertonia and dystonia of both handsCSF: 14-3-3(+); MRI: cortical atrophy and multiple white matter lesions. EEG: pseudo-periodic slow spike discharges; PRNP: N/A; Autopsy: CJDSporadic CJDPalliative carePassed away (4 months)
De Carvalho Neto et al[6]2019Male52CaucasianProgressive imbalance, motor and cognitive deterioration and hypersomniaCSF: 14-3-3(+); MRI: cortical gyri_x005f form restriction on both hemispheres; EEG: triphasic PSWC; PRNP: N/A; Autopsy: N/AProbable sporadic CJDPalliative carePassed away (greater than 2 months)
van de Ven et al[21]2019Male63Black ZimbabweanProgressive difficulties with decision-making, obsessive compulsive disorder and visual hallucinationsCSF: 14-3-3 (weakly+); MRI: bilateral abnormal signal within the posterolateral thalami compatible with pulvinar sign; EEG: Diffuse excess of slow activity; PRNP: M129V; Autopsy: CJDVariant CJDPalliative carePassed away (10 months)
Dahy et al[5]2021Male52BrazilGlobal cerebellar syndrome, bilateral Babinski, 4-limb paratonia and release of face axial reflexes. The memory, attention and executive function deficitsCSF: 14-3-3(+); MRI: bilateral hyper intensity of images in caudal nuclei; EEG: (-); PRNP: M129V; Autopsy: N/AProbable sporadic CJDN/APassed away (13 months)
Dahy et al[5]2021Male61BrazilAsthenia, lack of appetite, difficulty sleeping and occasional memory lapses, uncoordinated steps, visual delusions and bladder incontinenceCSF: 14-3-3(+); MRI: bilateral cortical ribboning in the cerebral cortex; PRNP: N/A; EEG: N/A; Autopsy: N/AProbable sporadic CJDN/APassed away (5 months)
Current report2022Male54Han/ChinaProgressive hypomnesis, paroxysmal anterograde amnesia, unsteady gaitCSF: 14-3-3 (weakly+); MRI: Bilateral abnormal signal within the posterolateral thalami compatible; EEG: Borderline abnormality of the periodic triphasic wave; PRNP: 129 M/M; Autopsy: N/AProbable ADCAnti-HIVImproved and following-up

The first patient was published by Babi et al[4] in 2016. The patient had well-controlled chronic AIDS. The elderly man passed away 3 months after a positive 14-3-3 protein test in the CSF, and a diagnosis of sCJD was confirmed histopathologically by autopsy. Subsequent reports indicate that all patients with similar conditions died within 2 months to 13 months[3,5-7,21]. In 3 of these cases, the diagnosis of sCJD was also confirmed by autopsy[3,7,21], and variant CJD in 1 case[21]. In the remaining 2 cases, autopsies were unavailable, but CJD was highly suspected[5,6]. The majority of these authors concur that there is no direct evidence linking HIV infection and prion diseases; however, further investigation is needed[4,6,7,21]. Abu-Rumeileh et al[3] concluded that RT-QuIC should be utilized as a specific screening tool for progressive dementia, while Dahy et al[5] contend that screening for sCJD should be mandatory in young patients with dementia who are living with HIV.

In our case, the patient's symptoms improved following anti-AIDS treatment, reducing the likelihood to be diagnosed with CJD (Table 1). Although 7 patients documented in previous reports shared similarities with the current case, presenting with AIDS and positive 14-3-3 protein, they were ultimately confirmed to have CJD via autopsy (Table 2).

In patients without routine HIV screening tests, RPD and positive 14-3-3 protein in CSF may easily lead to a misdiagnosis of CJD. Neurologists should exert every effort to determine the cause of RPD during diagnosis. Positive 14-3-3 protein expression is of great value in CJD diagnosis, but it also has some limitations and presents interference. Re-evaluation of the CSF 14-3-3 protein or an RT-QuIC test should be considered to enhance diagnostic accuracy when additional examinations are not available for such rare cases.


HAD and CJD are easily misdiagnosed. In the etiological diagnosis of RPD, it is vital to exclude as many causes as possible and, if necessary, perform an autopsy to minimize diagnostic bias. The 14-3-3 protein should not be regarded as the only marker for CJD. Comprehensive laboratory screening for infection markers is essential to enhance diagnostic precision, particularly in cases where AIDS coexists with CJD. Furthermore, a trial of diagnostic treatment may be beneficial when additional diagnostic tests are not accessible.


Provenance and peer review: Unsolicited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Clinical neurology

Country/Territory of origin: China

Peer-review report’s scientific quality classification

Grade A (Excellent): 0

Grade B (Very good): B

Grade C (Good): 0

Grade D (Fair): 0

Grade E (Poor): 0

P-Reviewer: Khosravi M, Iran S-Editor: Liu JH L-Editor: Filipodia P-Editor: Xu ZH

1.  McArthur JC, Brew BJ, Nath A. Neurological complications of HIV infection. Lancet Neurol. 2005;4:543-555.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 375]  [Cited by in F6Publishing: 349]  [Article Influence: 18.4]  [Reference Citation Analysis (0)]
2.  Sitammagari KK, Masood W.   Creutzfeldt Jakob Disease. 2024 Jan 30. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Abu-Rumeileh S, Capellari S, Parchi P. Rapidly Progressive Alzheimer's Disease: Contributions to Clinical-Pathological Definition and Diagnosis. J Alzheimers Dis. 2018;63:887-897.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 14]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
4.  Babi MA, Kraft BD, Sengupta S, Peterson H, Orgel R, Wegermann Z, Lugogo NL, Luedke MW. Related or not? Development of spontaneous Creutzfeldt-Jakob disease in a patient with chronic, well-controlled HIV: A case report and review of the literature. SAGE Open Med Case Rep. 2016;4:2050313X16672153.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 6]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
5.  Dahy FE, Novaes CTG, Bandeira GA, Ramin LF, Oliveira ACP, Smid J. Sporadic Creutzfeldt-Jakob disease in two clinically and virologically controlled Brazilian HIV patients who progressed rapidly to dementia: case reports and literature review. Rev Inst Med Trop Sao Paulo. 2021;63:e23.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
6.  De Carvalho Neto EG, Gomes MF, De Oliveira M, Guete MIN, Santos IP, Monteiro MD, Stelzer FG, Kowacs F, Barea LM. The worst is yet to come: probable sporadic Creutzfeldt-Jakob disease in a well-controlled HIV patient. Prion. 2019;13:156-159.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
7.  Eimer J, Vesterbacka J, Savitcheva I, Press R, Roshanisefat H, Nowak P. Nonopportunistic infection leading to rapidly progressive dementia in a patient with HIV/AIDS: A case report. Medicine (Baltimore). 2018;97:e0162.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
8.  Geschwind MD. Rapidly Progressive Dementia. Continuum (Minneap Minn). 2016;22:510-537.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 52]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
9.  Hermann P, Appleby B, Brandel JP, Caughey B, Collins S, Geschwind MD, Green A, Haïk S, Kovacs GG, Ladogana A, Llorens F, Mead S, Nishida N, Pal S, Parchi P, Pocchiari M, Satoh K, Zanusso G, Zerr I. Biomarkers and diagnostic guidelines for sporadic Creutzfeldt-Jakob disease. Lancet Neurol. 2021;20:235-246.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 68]  [Cited by in F6Publishing: 117]  [Article Influence: 39.0]  [Reference Citation Analysis (0)]
10.  Muayqil T, Gronseth G, Camicioli R. Evidence-based guideline: diagnostic accuracy of CSF 14-3-3 protein in sporadic Creutzfeldt-Jakob disease: report of the guideline development subcommittee of the American Academy of Neurology. Neurology. 2012;79:1499-1506.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 100]  [Cited by in F6Publishing: 97]  [Article Influence: 8.1]  [Reference Citation Analysis (0)]
11.  Franceschini A, Baiardi S, Hughson AG, McKenzie N, Moda F, Rossi M, Capellari S, Green A, Giaccone G, Caughey B, Parchi P. High diagnostic value of second generation CSF RT-QuIC across the wide spectrum of CJD prions. Sci Rep. 2017;7:10655.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 112]  [Cited by in F6Publishing: 121]  [Article Influence: 17.3]  [Reference Citation Analysis (0)]
12.  Lattanzio F, Abu-Rumeileh S, Franceschini A, Kai H, Amore G, Poggiolini I, Rossi M, Baiardi S, McGuire L, Ladogana A, Pocchiari M, Green A, Capellari S, Parchi P. Prion-specific and surrogate CSF biomarkers in Creutzfeldt-Jakob disease: diagnostic accuracy in relation to molecular subtypes and analysis of neuropathological correlates of p-tau and Aβ42 levels. Acta Neuropathol. 2017;133:559-578.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 102]  [Cited by in F6Publishing: 113]  [Article Influence: 16.1]  [Reference Citation Analysis (0)]
13.  Abu-Rumeileh S, Steinacker P, Polischi B, Mammana A, Bartoletti-Stella A, Oeckl P, Baiardi S, Zenesini C, Huss A, Cortelli P, Capellari S, Otto M, Parchi P. CSF biomarkers of neuroinflammation in distinct forms and subtypes of neurodegenerative dementia. Alzheimers Res Ther. 2019;12:2.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 77]  [Cited by in F6Publishing: 74]  [Article Influence: 14.8]  [Reference Citation Analysis (0)]
14.  Fiorini M, Iselle G, Perra D, Bongianni M, Capaldi S, Sacchetto L, Ferrari S, Mombello A, Vascellari S, Testi S, Monaco S, Zanusso G. High Diagnostic Accuracy of RT-QuIC Assay in a Prospective Study of Patients with Suspected sCJD. Int J Mol Sci. 2020;21.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 24]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
15.  Bizzi A, Pascuzzo R, Blevins J, Grisoli M, Lodi R, Moscatelli MEM, Castelli G, Cohen ML, Schonberger LB, Foutz A, Safar JG, Appleby BS, Gambetti P. Evaluation of a New Criterion for Detecting Prion Disease With Diffusion Magnetic Resonance Imaging. JAMA Neurol. 2020;77:1141-1149.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 27]  [Article Influence: 9.0]  [Reference Citation Analysis (0)]
16.  Forner SA, Takada LT, Bettcher BM, Lobach IV, Tartaglia MC, Torres-Chae C, Haman A, Thai J, Vitali P, Neuhaus J, Bostrom A, Miller BL, Rosen HJ, Geschwind MD. Comparing CSF biomarkers and brain MRI in the diagnosis of sporadic Creutzfeldt-Jakob disease. Neurol Clin Pract. 2015;5:116-125.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 43]  [Cited by in F6Publishing: 44]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
17.  Rudge P, Hyare H, Green A, Collinge J, Mead S. Imaging and CSF analyses effectively distinguish CJD from its mimics. J Neurol Neurosurg Psychiatry. 2018;89:461-466.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 62]  [Cited by in F6Publishing: 56]  [Article Influence: 9.3]  [Reference Citation Analysis (0)]
18.  Steinhoff BJ, Zerr I, Glatting M, Schulz-Schaeffer W, Poser S, Kretzschmar HA. Diagnostic value of periodic complexes in Creutzfeldt-Jakob disease. Ann Neurol. 2004;56:702-708.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 141]  [Cited by in F6Publishing: 116]  [Article Influence: 6.1]  [Reference Citation Analysis (0)]
19.  Yu SL, Jin L, Sy MS, Mei FH, Kang SL, Sun GH, Tien P, Wang FS, Xiao GF. Polymorphisms of the PRNP gene in Chinese populations and the identification of a novel insertion mutation. Eur J Hum Genet. 2004;12:867-870.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 37]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
20.  Joseph J, Colosi DA, Rao VR. HIV-1 Induced CNS Dysfunction: Current Overview and Research Priorities. Curr HIV Res. 2016;14:389-399.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 11]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
21.  van de Ven NS, Vera J, Jones JR, Vundavalli S, Ridha BH. Sporadic CJD in association with HIV. J Neurol. 2019;266:253-257.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]