Related Experiment Video

Updated: Aug 19, 2026

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Diffuse Lewy body disease

K Kosaka1

  • 1Department of Psychiatry, Yokohama City University, Yokohama, Kanagawa.

Internal Medicine (Tokyo, Japan)
|March 24, 1998
PubMed

Insights

Diagnosing diffuse Lewy body disease (DLBD) is challenging, despite it being the second most common dementia. Continued research for diagnostic markers is crucial for accurate identification of dementia with Lewy bodies.

Area of Science:

  • Neurology
  • Pathology

Background:

  • Diffuse Lewy body disease (DLBD) is a significant cause of dementia in the elderly, second only to Alzheimer's disease.
  • Clinical diagnosis of DLBD is often difficult, leading to frequent misdiagnoses.
  • A unified term, dementia with Lewy bodies (DLB), now encompasses DLBD and related conditions.

Purpose of the Study:

  • To highlight the diagnostic challenges associated with DLBD.
  • To emphasize the ongoing need for reliable diagnostic markers for DLB.
  • To introduce the pathological hallmark of DLB: cortical Lewy bodies.

Main Methods:

  • Review of existing literature on DLBD and DLB.
  • Analysis of clinical diagnostic criteria and their limitations.
  • Discussion of pathological findings, specifically cortical Lewy bodies.

Main Results:

  • DLBD is frequently misdiagnosed clinically.
  • Cortical Lewy bodies are the key pathological feature for DLB diagnosis.
  • The precise mechanism of cortical Lewy body formation remains unknown.

Conclusions:

  • Accurate clinical diagnosis of DLBD remains a significant challenge.
  • The identification of diagnostic markers for DLB is a critical area for continued research.
  • Understanding the pathogenesis of cortical Lewy bodies is essential for advancing DLB diagnosis and treatment.

More Related Videos

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons10:03

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Technique for Intranasal Administration of α-Synuclein Aggregates04:49

Technique for Intranasal Administration of α-Synuclein Aggregates

Published on: November 8, 2024

Related Concept Videos

Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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 microglia. Abnormal...
Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of which...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...