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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...
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...
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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...

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Related Experiment Video

Updated: Jul 16, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Calcium and neurodegeneration.

Mark P Mattson1

  • 1Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA. mattsonm@grc.nia.nih.gov

Aging Cell
|March 3, 2007
PubMed
Summary

Calcium (Ca2+) regulation is vital for neuron function but declines with aging and neurodegenerative diseases. Understanding these disruptions may reveal new therapeutic targets for conditions like Alzheimer's and Parkinson's.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Calcium (Ca2+) signaling is essential for neuronal functions like synaptic plasticity and survival.
  • Aging and neurodegenerative diseases impair cellular Ca2+ regulation, leading to synaptic dysfunction and neuronal degeneration.

Purpose of the Study:

  • To elucidate the mechanisms by which aging and neurodegenerative diseases disrupt neuronal Ca2+ homeostasis.
  • To identify Ca2+-regulating proteins and pathways affected in neurological disorders.

Main Methods:

  • Review and synthesis of recent findings on Ca2+ homeostasis in aging and neurodegeneration.
  • Analysis of alterations in Ca2+-regulating proteins in plasma membrane, endoplasmic reticulum, and mitochondria.
  • Examination of genetic and environmental factors influencing neuronal Ca2+ regulation.

More Related Videos

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
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Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis

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Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans
07:04

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans

Published on: August 15, 2020

Related Experiment Videos

Last Updated: Jul 16, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
11:42

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis

Published on: November 20, 2013

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans
07:04

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans

Published on: August 15, 2020

Main Results:

  • Oxidative stress, metabolic dysfunction, and protein aggregation disrupt Ca2+ homeostasis.
  • Specific Ca2+-regulating proteins in various cellular compartments are implicated in age-related neuronal dysfunction.
  • Genetic and environmental factors modify the impact of aging on neuronal Ca2+ regulation.

Conclusions:

  • Dysregulation of Ca2+ homeostasis is a key factor in age-related neuronal dysfunction and neurodegenerative diseases.
  • Targeting cellular Ca2+ regulatory systems offers potential therapeutic strategies for neurological disorders.
  • Further understanding of these mechanisms can guide novel interventions for Alzheimer's, Parkinson's, and stroke.