Role of Apoptosis in disease

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Abstract

Since the initial description of apoptosis, a number of different forms of cell death have been described. In this review we will focus on classic caspase-dependent apoptosis and its variations that contribute to diseases. Over fifty years of research have clarified molecular mechanisms involved in apoptotic signaling as well and shown that alterations of these pathways lead to human diseases. Indeed both reduced and increased apoptosis can result in pathology. More recently these findings have led to the development of therapeutic approaches based on regulation of apoptosis, some of which are in clinical trials or have entered medical practice.

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Most cited references 182

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Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation.

M E Gurney, H Pu, A Y Chiu … (1994)

Mutations of human Cu,Zn superoxide dismutase (SOD) are found in about 20 percent of patients with familial amyotrophic lateral sclerosis (ALS). Expression of high levels of human SOD containing a substitution of glycine to alanine at position 93--a change that has little effect on enzyme activity--caused motor neuron disease in transgenic mice. The mice became paralyzed in one or more limbs as a result of motor neuron loss from the spinal cord and died by 5 to 6 months of age. The results show that dominant, gain-of-function mutations in SOD contribute to the pathogenesis of familial ALS.

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Classification and basic pathology of Alzheimer disease.

Charles Duyckaerts, Benoît Delatour, Marie-Claude Potier (2009)

The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Abeta accumulation occurs in the parenchyma as diffuse, focal or stellate deposits. It may involve the vessel walls of arteries, veins and capillaries. The cases in which the capillary vessel walls are affected have a higher probability of having one or two apoepsilon 4 alleles. Parenchymal as well as vascular Abeta deposition follows a stepwise progression. Tau accumulation, probably the best histopathological correlate of the clinical symptoms, takes three aspects: in the cell body of the neuron as neurofibrillary tangle, in the dendrites as neuropil threads, and in the axons forming the senile plaque neuritic corona. The progression of tau pathology is stepwise and stereotyped from the entorhinal cortex, through the hippocampus, to the isocortex. The neuronal loss is heterogeneous and area-specific. Its mechanism is still discussed. The timing of the synaptic loss, probably linked to Abeta peptide itself, maybe as oligomers, is also controversial. Various clinico-pathological types of Alzheimer disease have been described, according to the type of the lesions (plaque only and tangle predominant), the type of onset (focal onset), the cause (genetic or sporadic) and the associated lesions (Lewy bodies, vascular lesions, hippocampal sclerosis, TDP-43 inclusions and argyrophilic grain disease).

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Amyotrophic lateral sclerosis (ALS) is a paralytic disorder caused by motor neuron degeneration. Mutations in more than 50 human genes cause diverse types of motor neuron pathology. Moreover, defects in five Mendelian genes lead to motor neuron disease, with two mutations reproducing the ALS phenotype. Analyses of these genetic effects have generated new insights into the diverse molecular pathways involved in ALS pathogenesis. Here, we present an overview of the mechanisms for motor neuron death and of the role of non-neuronal cells in ALS.

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Author and article information

Journal

Journal ID (nlm-ta): Aging (Albany NY)

Journal ID (iso-abbrev): Aging (Albany NY)

Journal ID (publisher-id): ImpactJ

Title: Aging (Albany NY)

Publisher: Impact Journals LLC

ISSN (Electronic): 1945-4589

Publication date Collection: May 2012

Publication date (Electronic): 31 May 2012

Volume: 4

Issue: 5

Pages: 330-349

Affiliations

¹ Dipartimento di Scienze Biomediche, Universita' “G. d'Annunzio” Chieti-Pescara, 66100, Chieti, Italy

² Fondazione “G. d'Annunzio”, Centro Studi sull'Invecchiamento, Ce.S.I., 66100, Chieti, Italy

³ BIOUNIVERSA srl, University of Salerno, Fisciano (SA), Italy

Author notes

Correspondence to: Vincenzo De Laurenzi, PhD; delaurenzi@ 123456unich.it

Article

DOI: 10.18632/aging.100459

PMC ID: 3384434

PubMed ID: 22683550

SO-VID: 4c2d407f-e04c-425d-ae00-a9de1b17ce10

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

History

Date received : 15 May 2012

Date accepted : 30 May 2012

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