Related Experiment Video

Updated: Aug 8, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

NAD+ and NADH in cellular functions and cell death

Weihai Ying1

  • 1Department of Neurology, University of California, San Francisco Veterans Affairs Medical Center, San Francisco, CA 94121, USA. Weihai.Ying@ucsf.edu

Frontiers in Bioscience : a Journal and Virtual Library
|May 25, 2006
PubMed

Insights

Nicotinamide adenine dinucleotide (NAD+) and its reduced form (NADH) are vital for cellular functions, energy metabolism, and aging. Intranasal NAD+ administration shows promise in reducing brain damage, suggesting new therapeutic avenues.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Aging Research

Background:

  • NAD+ and NADH are crucial for energy metabolism, cell death, calcium homeostasis, and gene expression.
  • These molecules regulate key enzymes like sirtuins and PARPs, implicated in aging and cellular functions.
  • Emerging evidence suggests extracellular NAD+ acts as a signaling molecule and can be transported across cell membranes.

Purpose of the Study:

  • To explore the multifaceted roles of NAD+ and NADH in biological processes.
  • To investigate the potential of NAD+ as a therapeutic agent for conditions like ischemic brain damage.
  • To propose a new paradigm for understanding NAD+ and NADH metabolism and activity.

Main Methods:

  • Review of existing literature on NAD+ and NADH functions.
  • Analysis of NAD+/NADH-dependent enzymes and their roles.
  • Presentation of recent findings on intranasal NAD+ administration in reducing ischemic brain damage.

Main Results:

  • NAD+ and NADH regulate critical cellular processes, including calcium signaling via TRPM2 and ryanodine receptors.
  • Sirtuins and PARPs, NAD+-dependent enzymes, are key players in aging and cell death.
  • Intranasal NAD+ administration significantly reduced ischemic brain damage in studies.

Conclusions:

  • NAD+ and NADH are fundamental molecules influencing nearly all major biological processes, potentially alongside ATP and Ca2+.
  • Further research into NAD+ and NADH could unlock new strategies for combating aging and various diseases.
  • Extracellular NAD+ represents a novel signaling pathway with therapeutic implications.

More Related Videos

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...