Editing Mitochondrial disease (section)

===Associated conditions===
Acquired conditions in which mitochondrial dysfunction has been involved include:
* [[ALS]]<ref>{{cite journal |last1=Muyderman |first1=H |last2=Chen |first2=T |date=April 2014 |title=Mitochondrial dysfunction in amyotrophic lateral sclerosis – a valid pharmacological target? |journal=British Journal of Pharmacology |volume=171 |issue=8 |pages=2191–2205 |doi=10.1111/bph.12476 |pmc=3976630 |pmid=24148000}}</ref>
* [[Alzheimer's disease]],<ref>{{cite journal |last1=Abyadeh |first1=Morteza |last2=Gupta |first2=Vivek |last3=Chitranshi |first3=Nitin |last4=Gupta |first4=Veer |last5=Wu |first5=Yunqi |last6=Saks |first6=Danit |last7=WanderWall |first7=Roshana |last8=Fitzhenry |first8=Matthew J |last9=Basavarajappa |first9=Devaraj |last10=You |first10=Yuyi |last11=H Hosseini |first11=Ghasem |last12=A Haynes |first12=Paul |last13=L Graham |first13=Stuart |last14=Mirzaei |first14=Mehdi |year=2021 |title=Mitochondrial dysfunction in Alzheimer's disease - a proteomics perspective |journal=Expert Review of Proteomics |volume=18 |issue=4 |pages=295–304 |doi=10.1080/14789450.2021.1918550 |pmid=33874826 |s2cid=233310698}}</ref>
* [[Bipolar disorder]],<ref>{{cite journal |last1=Stork |first1=C |last2=Renshaw |first2=P F |year=2005 |title=Mitochondrial dysfunction in bipolar disorder: Evidence from magnetic resonance spectroscopy research |journal=Molecular Psychiatry |volume=10 |issue=10 |pages=900–19 |doi=10.1038/sj.mp.4001711 |pmid=16027739 |doi-access=free}}</ref><ref name="ReferenceA">{{cite journal |last1=Pieczenik |first1=Steve R |last2=Neustadt |first2=John |year=2007 |title=Mitochondrial dysfunction and molecular pathways of disease |journal=Experimental and Molecular Pathology |volume=83 |issue=1 |pages=84–92 |doi=10.1016/j.yexmp.2006.09.008 |pmid=17239370}}</ref><ref>{{cite journal |last1=Nierenberg |first1=Andrew A |last2=Kansky |first2=Christine |last3=Brennan |first3=Brian P |last4=Shelton |first4=Richard C |last5=Perlis |first5=Roy |last6=Iosifescu |first6=Dan V |year=2012 |title=Mitochondrial modulators for bipolar disorder: A pathophysiologically informed paradigm for new drug development |journal=Australian & New Zealand Journal of Psychiatry |volume=47 |issue=1 |pages=26–42 |doi=10.1177/0004867412449303 |pmid=22711881 |s2cid=22983555}}</ref> [[schizophrenia]], aging and senescence,<ref>{{cite journal |last1=Valiente-Pallejà |first1=A |last2=Tortajada |first2=J |last3=Bulduk |first3=BK |year=2022 |title=Comprehensive summary of mitochondrial DNA alterations in the postmortem human brain: A systematic review |journal=eBioMedicine |volume=76 |issue=103815 |page=103815 |doi=10.1016/j.ebiom.2022.103815 |pmc=8790490 |pmid=35085849 |doi-access=free}}</ref> anxiety disorders<ref>{{cite journal |last1=Misiewicz |first1=Zuzanna |last2=Iurato |first2=Stella |last3=Kulesskaya |first3=Natalia |last4=Salminen |first4=Laura |last5=Rodrigues |first5=Luis |last6=Maccarrone |first6=Giuseppina |last7=Martins |first7=Jade |last8=Czamara |first8=Darina |last9=Laine |first9=Mikaela A. |last10=Sokolowska |first10=Ewa |last11=Trontti |first11=Kalevi |last12=Rewerts |first12=Christiane |last13=Novak |first13=Bozidar |last14=Volk |first14=Naama |last15=Park |first15=Dong Ik |date=26 September 2019 |title=Multi-omics analysis identifies mitochondrial pathways associated with anxiety-related behavior |journal=PLOS Genetics |volume=15 |issue=9 |pages=e1008358 |doi=10.1371/journal.pgen.1008358 |pmc=6762065 |pmid=31557158 |doi-access=free |last16=Jokitalo |first16=Eija |last17=Paulin |first17=Lars |last18=Auvinen |first18=Petri |last19=Voikar |first19=Vootele |last20=Chen |first20=Alon |last21=Erhardt |first21=Angelika |last22=Turck |first22=Christoph W. |last23=Hovatta |first23=Iiris}}</ref>
* [[Cancer]]
* [[Cardiovascular disease]]
* [[Diabetes]]
* [[Huntington's disease]]
* [[Long Covid]]
* [[ME/CFS]]
* [[Parkinson's disease]]
* [[Sarcopenia]]<ref name="ReferenceA" />

The body, and each mutation, is modulated by other genome variants; the mutation that in one individual may cause liver disease might in another person cause a brain disorder. The severity of the specific defect may also be great or small. Some defects include [[exercise intolerance]]. Defects often affect the operation of the mitochondria and multiple tissues more severely, leading to multi-system diseases.<ref name="pmid22424226">{{cite journal |vauthors = Nunnari J, Suomalainen A |title = Mitochondria: in sickness and in health |journal = Cell |volume = 148 |issue = 6 |pages = 1145–59 |year = 2012 |pmid = 22424226 |pmc = 5381524 |doi = 10.1016/j.cell.2012.02.035 }}</ref>

It has also been reported that drug tolerant cancer cells have an increased number and size of mitochondria, which suggested an increase in mitochondrial biogenesis.<ref name="pmid31431543">{{cite journal | vauthors = Goldman A, Khiste S, Freinkman E, Dhawan A, Majumder B, Mondal J, Pinkerton AB, Eton E, Medhi R, Chandrasekar V, Rahman MM, Ichimura T, Gopinath KS, Majumder P, Kohandel M, Sengupta S | display-authors = 6 | title = Targeting tumor phenotypic plasticity and metabolic remodeling in adaptive cross-drug tolerance | journal = Science Signaling | volume = 12 | issue = 595 | date = August 2019 | pmid = 31431543 | doi = 10.1126/scisignal.aas8779 | pmc = 7261372 }}</ref> A recent study in ''Nature Nanotechnology'' has reported that cancer cells can hijack the mitochondria from immune cells via physical tunneling nanotubes.<ref>{{cite journal | vauthors = Saha T, Dash C, Jayabalan R, etal | title = Intercellular nanotubes mediate mitochondrial trafficking between cancer and immune cells. | journal = Nat. Nanotechnol. |  date = 2021  | volume = 17 | issue = 1 | pages = 98–106 | doi = 10.1038/s41565-021-01000-4  | pmid = 34795441 | s2cid = 244349825 | pmc = 10071558 }}</ref>

As a rule, mitochondrial diseases are worse when the defective mitochondria are present in the [[muscle]]s, [[cerebrum]], or [[nerve]]s,<ref name=pmid17637511>{{cite journal |doi=10.1159/000105676 |pmid=17637511 |title=Hematological Manifestations of Primary Mitochondrial Disorders |journal=Acta Haematologica |volume=118 |issue=2 |pages=88–98 |year=2007 |last1=Finsterer |first1=Josef |s2cid=24222021 }}</ref> because these cells use more energy than most other cells in the body.

Although mitochondrial diseases vary greatly in presentation from person to person, several major clinical categories of these conditions have been defined, based on the most common phenotypic features, symptoms, and signs associated with the particular mutations that tend to cause them.{{citation needed|date=October 2017}}

An outstanding question and area of research is whether ATP depletion or reactive oxygen species are in fact responsible for the observed phenotypic consequences.{{citation needed|date=October 2017}}

Cerebellar atrophy or [[cerebellar hypoplasia|hypoplasia]] has sometimes been reported to be associated.<ref>{{cite journal |doi=10.1097/NEN.0b013e318244477d |pmid=22249460 |pmc=3272439 |title=Cerebellar Ataxia in Patients with Mitochondrial DNA Disease |journal=Journal of Neuropathology & Experimental Neurology |volume=71 |issue=2 |pages=148–61 |year=2012 |last1=Lax |first1=Nichola Zoe |last2=Hepplewhite |first2=Philippa Denis |last3=Reeve |first3=Amy Katherine |last4=Nesbitt |first4=Victoria |last5=McFarland |first5=Robert |last6=Jaros |first6=Evelyn |last7=Taylor |first7=Robert William |last8=Turnbull |first8=Douglass Matthew }}</ref>