Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

The Shortening of Leukocyte Telomere Length Contributes to Alzheimer’s Disease: Further Evidence from Late-Onset Familial and Sporadic Cases

Paolina Crocco
ORCID logo ,
Francesco De Rango
,
Serena Dato
,
Rossella La Grotta
,
Raffaele Maletta
,
Amalia Cecilia Bruni
,
Giuseppe Passarino
ORCID logo ,
Giuseppina Rose
* ORCID logo
Version 1 : Received: 22 August 2023 / Approved: 22 August 2023 / Online: 22 August 2023 (13:22:03 CEST)

A peer-reviewed article of this Preprint also exists.

Crocco, P.; De Rango, F.; Dato, S.; La Grotta, R.; Maletta, R.; Bruni, A.C.; Passarino, G.; Rose, G. The Shortening of Leukocyte Telomere Length Contributes to Alzheimer’s Disease: Further Evidence from Late-Onset Familial and Sporadic Cases. Biology 2023, 12, 1286. Crocco, P.; De Rango, F.; Dato, S.; La Grotta, R.; Maletta, R.; Bruni, A.C.; Passarino, G.; Rose, G. The Shortening of Leukocyte Telomere Length Contributes to Alzheimer’s Disease: Further Evidence from Late-Onset Familial and Sporadic Cases. Biology 2023, 12, 1286.

Abstract

Telomeres are structures at the ends of eukaryotic chromosomes that help maintain genomic stability. During aging, telomere length gradually shortens, producing short telomeres, which are considered markers of premature cellular senescence. This is believed to contribute to age-related diseases, including Alzheimer's disease (AD) and based on this, several studies have hypothesized that telomere shortening may characterize AD. Current research, however, has been inconclusive regarding the direction of the association between leukocyte telomere length (LTL) and disease risk. We assessed the association between LTL and AD in a retrospective case-control study of a sample of 255 unrelated patients with late-onset AD (LOAD), including 120 sporadic cases and 135 with positive family history for LOAD, and a group of 279 cognitively healthy unrelated controls, which were all from Calabria, a region from south Italy. Following regression analysis, telomeres were found to be significantly shorter in LOAD cases than in controls (p<0.001 for both sporadic and familial cases). Interestingly, LTL were associated to disease risk independently of the presence of conventional risk factors (e.g., age, sex, MMSE scores, presence of the APOE-ε4 allele). Altogether, our findings lend support to the notion that LTL shortening may be an indicator of the patho-genesis of LOAD.

Keywords

Telomere length; Telomeres; Alzheimer’s Disease; late-onset AD, Aging, Neurodegeneration

Subject

Biology and Life Sciences, Aging

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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