Related Experiment Video

Updated: Jul 17, 2026

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

Alzheimer's disease is a synaptic failure

Dennis J Selkoe1

  • 1Center for Neurologic Diseases, Brigham and Women's Hospital, and the Harvard Center for Neurodegeneration and Repair, Boston, MA 02115, USA. selkoe@cnd.bwh.harvard.edu

Science (New York, N.Y.)
|October 26, 2002
PubMed

Insights

Early Alzheimer's disease impairs memory due to synaptic changes in the hippocampus. These synaptic dysfunctions are linked to amyloid beta protein

Area of Science:

  • Neuroscience
  • Neurology
  • Pathology

Background:

  • Alzheimer's disease (AD) initially presents as pure memory impairment.
  • Evidence points to hippocampal synaptic alterations preceding neuronal loss in early AD.

Purpose of the Study:

  • To investigate the early molecular mechanisms underlying memory deficits in Alzheimer's disease.
  • To explore the role of amyloid beta in synaptic dysfunction.

Main Methods:

  • Analysis of synaptic efficacy in hippocampal models.
  • Investigation of diffusible oligomeric assemblies of amyloid beta protein.

Main Results:

  • Subtle alterations in hippocampal synaptic efficacy characterize early AD.
  • Synaptic dysfunction is associated with amyloid beta oligomers.

Conclusions:

  • Amyloid beta oligomers are implicated in the synaptic dysfunction observed in early Alzheimer's disease.
  • Targeting amyloid beta may offer therapeutic strategies for early AD memory loss.

More Related Videos

Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation07:17

Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation

Published on: August 23, 2024

Visualizing the DNA Damage Response in Purkinje Cells Using Cerebellar Organotypic Cultures08:41

Visualizing the DNA Damage Response in Purkinje Cells Using Cerebellar Organotypic Cultures

Published on: December 27, 2024

Related Concept Videos

Disorders of the Nervous Tissue01:28

Disorders of the Nervous Tissue

Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises from the...
American Trypanosomiasis01:22

American Trypanosomiasis

Chagas disease, or American trypanosomiasis, is a vector-borne parasitic infection caused by Trypanosoma cruzi, a flagellated protozoan (kinetoplastid) of the family Trypanosomatidae. The disease is endemic in Latin America, although cases are increasingly reported worldwide due to human migration. Transmission most commonly occurs when feces of infected triatomine bugs contaminate bite wounds or mucosal surfaces; additional routes include congenital, transfusional, transplant-related, and oral...
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...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
Esophageal Achalasia01:27

Esophageal Achalasia

Esophageal achalasia is a chronic neurogenic disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and absent or ineffective peristalsis in the distal esophagus. This leads to a functional obstruction without a physical blockage, despite significant disruption of esophageal motility.EtiologyAchalasia is caused by degeneration of the myenteric (Auerbach's) plexus, specifically the loss of inhibitory ganglion cells that produce vasoactive intestinal peptide (VIP)...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...