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Related Concept Videos

Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
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The Effect of Aging on Tissues

Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
Pharmacodynamics in Geriatric Patients: Effects of Age01:27

Pharmacodynamics in Geriatric Patients: Effects of Age

Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...
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

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Related Experiment Video

Updated: Jun 27, 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

Docosahexaenoic acid and the aging brain.

Walter J Lukiw1, Nicolas G Bazan

  • 1Department of Ophthalmology, LSU Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA. wlukiw@lsuhsc.edu

The Journal of Nutrition
|November 22, 2008
PubMed
Summary

Docosahexaenoic acid (DHA) and its derivative neuroprotectin D1 (NPD1) are vital for brain health, influencing neuroprotection and Alzheimer's disease (AD) pathology. Deficits in DHA/NPD1 are linked to cognitive decline and AD progression.

Related Experiment Videos

Last Updated: Jun 27, 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

Area of Science:

  • Neuroscience
  • Biochemistry
  • Molecular Biology

Background:

  • Docosahexaenoic acid (DHA) is essential for nervous system structure and function.
  • DHA deficits correlate with cognitive decline and neurodegenerative diseases.
  • Neuroprotectin D1 (NPD1), derived from DHA, plays a role in brain cell survival and repair.

Purpose of the Study:

  • To review the interactions between DHA, NPD1, and Alzheimer's disease (AD) pathology.
  • To explore the role of DHA and NPD1 in beta-amyloid precursor protein (betaAPP) processing and signaling.
  • To understand how these interactions contribute to aging and AD pathogenesis.

Main Methods:

  • Literature review of recent studies on DHA, NPD1, and AD.
  • Analysis of molecular-genetic mechanisms involving betaAPP and amyloid beta (Abeta).
  • Examination of signaling pathways related to inflammation, apoptosis, and oxidative stress.

Main Results:

  • NPD1 synthesis is activated by growth factors and neurotrophins.
  • NPD1 interacts with molecular mechanisms of betaAPP processing and Abeta peptide neurobiology.
  • DHA deficits or peroxidation contribute to inflammation, apoptosis, and neuronal dysfunction in AD.

Conclusions:

  • DHA and NPD1 are critical in regulating betaAPP processing and Abeta signaling.
  • Dysregulation of DHA and NPD1 contributes to the oxidative and pathogenic processes in aging and AD.
  • Further research into DHA and NPD1 pathways may offer therapeutic targets for AD.