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Related Concept Videos

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...
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...
Brainstem01:19

Brainstem

The brainstem, located inferior to the brain and superior to the spinal cord, serves as a bridge between the cerebrum and the spinal cord. It plays a vital role in relaying information and controlling critical life functions. It comprises three primary regions: the midbrain, pons, and medulla oblongata.
The Midbrain
The midbrain is located beneath the diencephalon and connects the cerebrum with the lower parts of the brain. The cerebral peduncles are prominent midbrain structures that house the...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Brainstem: Control Centers of Medulla01:21

Brainstem: Control Centers of Medulla

The medulla oblongata is a crucial part of the brainstem responsible for controlling various autonomic and involuntary functions. It contains several nuclei, including the olivary, cuneate, gracile, and solitary nuclei.
Olivary Nucleus
The olivary nucleus, or inferior olivary nucleus, is located within the ventrolateral part of the medulla oblongata. It is primarily involved in motor coordination and motor learning. The olivary nucleus receives input from the spinal cord, cerebellum, and motor...

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Related Experiment Video

Updated: Jun 21, 2026

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

Does Alzheimer's disease begin in the brainstem?

G Simic1, G Stanic, M Mladinov

  • 1Department of Neuroscience, Croatian Institute for Brain Research, Medical School Zagreb, Croatia. gsimic@hiim.hr

Neuropathology and Applied Neurobiology
|August 18, 2009
PubMed
Summary

Alzheimer's disease (AD) may begin in the brainstem's dorsal raphe nucleus (DRN), not just the hippocampus. This early involvement could explain non-cognitive symptoms and suggests oxidative damage as a key factor.

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A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease
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Published on: June 13, 2025

Related Experiment Videos

Last Updated: Jun 21, 2026

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease
05:39

A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease

Published on: June 13, 2025

Area of Science:

  • Neuroscience
  • Pathology
  • Gerontology

Background:

  • Alzheimer's disease (AD) severity correlates with neuronal cytoskeleton changes, but their origin and progression remain unclear.
  • Current AD diagnostic criteria focus on cognitive deficits, often overlooking early non-cognitive symptoms like mood and sleep disturbances.
  • These non-cognitive symptoms suggest potential involvement of brainstem nuclei, specifically serotonergic pathways.

Purpose of the Study:

  • To propose a novel pathogenetic scheme for Alzheimer's disease (AD) progression.
  • To investigate the potential early involvement of the dorsal raphe nucleus (DRN) in AD pathogenesis.
  • To explore the role of oxidative damage in the development of AD-related neuropathology.

Main Methods:

  • Review of recent reports on the involvement of raphe nuclei in AD.
  • Analysis of differential susceptibility and anatomical connectivity of brainstem nuclei.
  • Speculation on the role of cumulative oxidative damage in DRN alterations.

Main Results:

  • Evidence suggests selective and early involvement of raphe nuclei, particularly the dorsal raphe nucleus (DRN), in AD.
  • The dorsal raphe nucleus (DRN) may be an initial site for pathological changes in Alzheimer's disease (AD).
  • Age-related cumulative oxidative damage is hypothesized as a primary cause of DRN alterations in sporadic AD.

Conclusions:

  • The dorsal raphe nucleus (DRN) may represent an early site of pathology in Alzheimer's disease (AD) progression.
  • Oxidative damage is proposed as a key factor in the pathogenesis of AD, particularly in the DRN.
  • A revised understanding of AD progression, including brainstem involvement, is necessary for comprehensive diagnosis and treatment.