DLB vs PDD vs MSA tail (Aβ / NFT / GWAS / GBA / SNCA / CSF αsyn / Clinical trial), MSA agent registry (Lithium / Stem cell / Mesenex αSyn immunotx / Bicheron verepinstat), DNA damage section opener (definition / Causes / Type-Repair table opener / Consequence DDR / Major pathways of DNA repair table opener)

DLB vs PDD vs MSA — Clinical trial implications

Genetic / clinical trial
Lithium	NCT04299672
Stem cell	NCT01005365
Mesenex (2020 #800)	Mesenchymal αSyn immunotx
NCT00227968	Bicheron / vesperinstat / α-syn immunoTx (NCT02227968)
Bicheron: vespernstat is primarily a modified UMSARS, TBNG OF A SUBSET OF ITEMS FROM umsars PART 1 & 2

definition

a change in the basic structure of DNA that is not itself replicated when the DNA is replicated

ROS, reactive nitrogen species, reactive carbonyl species, lipid peroxidation products and alkylating agents, among others, while hydrolysis cleaves chemical bonds in DNA[8]
Naturally occurring oxidative DNA damages arise at least 10,000 times per cell per day in humans and as much as 100,000 per cell per day in rats[9] as documented below.
Other types of endogenous DNA damages, given below with their frequencies of occurrence, include depurinations, depyrimidinations, double-strand breaks, O6-methylguanines and cytosine deamination.
DNA can be damaged via environmental factors as well. Environmental agents such as UV light, ionizing radiation, and genotoxic chemicals. Replication forks can be stalled due to damaged DNA and double-strand breaks are also a source of damage [13]

type	(Steady-state) amounts of endogenous DNA damages per cell, per day	Repair process
Abasic site (AP site) (i.e. a base missing from the backbone of DNA) A DNA strand also (also in RNA but much less likely) that has neither a purine nor a pyrimidine base.	32,000	A DNA glycosylase (mammalian cells express as many as 11 distinct DNA glycosylases with overlapping substrate specificity) recognizes a damaged base and cleaves the N-glycosidic bond to release the base, leaving an AP site. A variety of glycosylases that recognize different types of damage exist, including oxidized or methylated bases, or uracil in DNA. → The AP site can then be cleaved by an AP endonuclease, leaving 3' hydroxyl and 5' deoxyribosephosphate termini (see DNA structure). (In alternative fashion, bifunctional glycosylase-lyases can cleave the AP site, leaving 3' phosphate adjacent to a 3' α,β-unsaturated aldehyde. → Both responses produce a single-strand break, which is then repaired by either short-patch or long-patch base excision repair[4]
a break in a strand of DNA, a chemically changed base such as 8-OH-dG.


DNA damage response (DDR) is a complex signal transduction pathway which recognizes when DNA is damaged and initiates the cellular response to the damage [7]	abnormal \| prevents the replication mechanism from functioning and replicating properly[1] Un-repaired DNA damages accumulate in non-replicating cells, such as cells in the brains and can cause aging.[2][3][4]

Repair pathway	Lesions	Accuracy	Ref.
Base excision repair	corrects DNA damage from oxidation, deamination and alkylation, also single-strand breaks oxidative endogenous lesions such as cyclopurine, sunlight-induced thymine dimers (cyclobutane dimers and pyrimidine 6-pyrimidone photoproducts)	accurate	[38]
Homology-directed repair	double-strand breaks if cells are in the G0 phase, the G1 phase or the G2 phase of the cell cycle	somewhat inaccurate	[38]
Non-homologous end joining	double-strand breaks if cells are in the G0 phase, the G1 phase or the G2 phase of the cell cycle	somewhat inaccurate	[38]
Microhomology-mediated end joining or alt-End joining	double-strand breaks in the S phase of the cell cycle	always inaccurate	[38]