Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

10.2K
Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
10.2K
Amyloid Fibrils03:03

Amyloid Fibrils

5.2K
5.2K
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

21
A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial...
21
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

35
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
35
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

21
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
21
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

22
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
22

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Radiotherapy-associated pleomorphic dermal sarcoma 33 years after basal cell carcinoma treatment.

JAAD case reports·2026
Same author

Staphylococcus aureus bacteremia: clinical outcomes and predictors of 28-day mortality in a tertiary-care cohort.

BMC infectious diseases·2026
Same author

Isolated Hematogenous Dissemination in Malignant Melanoma: Investigation of Potential Risk Factors.

Annals of plastic surgery·2026
Same author

Outcomes of Vascular Interventions in Takayasu Arteritis and the Role of Biologic Therapy: A Multicenter Retrospective Study.

International journal of rheumatic diseases·2026
Same author

An Extremely Rare and Devastating Complication of Penetrating Keratoplasty: Postoperative Endophthalmitis Because of Carbapenem-Resistant Klebsiella pneumoniae.

Eye & contact lens·2026
Same author

Juvenile Xanthogranuloma in a Congenital Melanocytic Nevus.

Dermatology practical & conceptual·2026

Related Experiment Video

Updated: May 2, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

6.8K

Primary systemic Al amyloidosis presenting as temporal arteritis.

Hakan Emmungil1, Melike Kalfa2, Burcu Başarık3

  • 1Mersin State Hospital, Department of Internal Medicine, Division of Rheumatology, Nusratiye Hometown, Kuvayi Milliye Street No. 32, 33050, Turkey.

Case Reports in Rheumatology
|February 20, 2014
PubMed
Summary

Giant cell arteritis (GCA) can mimic other conditions. A case highlights that while temporal artery biopsy is key for GCA, AL amyloidosis can present similarly, necessitating further diagnostic investigation.

More Related Videos

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

7.2K

Related Experiment Videos

Last Updated: May 2, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

6.8K
Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

7.2K

Area of Science:

  • Rheumatology
  • Internal Medicine
  • Pathology

Background:

  • Giant cell arteritis (GCA) is the most common form of vasculitis in the elderly.
  • GCA often presents with non-specific symptoms, mimicking various other disorders.
  • Temporal artery biopsy is the established gold standard for diagnosing GCA.

Purpose of the Study:

  • To report a case where initial symptoms suggested temporal arteritis.
  • To highlight the diagnostic challenge posed by AL amyloidosis presenting similarly to GCA.
  • To emphasize the importance of definitive diagnostic procedures in suspected GCA cases.

Main Methods:

  • Case report of a 67-year-old male patient.
  • Initial presentation evaluated for temporal arteritis.
  • Subsequent diagnostic procedures including lip biopsy.

Main Results:

  • The patient initially presented with symptoms consistent with temporal arteritis.
  • A lip biopsy ultimately revealed AL amyloidosis, not GCA.
  • This case underscores the potential for diagnostic confusion.

Conclusions:

  • Temporal artery biopsy remains crucial for definitive GCA diagnosis, especially in patients with systemic symptoms or treatment resistance.
  • AL amyloidosis can present with overlapping symptoms, necessitating a broad differential diagnosis.
  • Careful consideration of alternative diagnoses and appropriate biopsy selection are vital for accurate patient management.