Basic Explainatory Guide on Neurodegenerative Disorder

by Kyle A. Ragner

Nurdgnrt–n" – a mmnl used wrd wh mn–ng – bl–vd t be un–vrll understood. Yet f–nd–ng a r– df–n–t–n for neurodegeneration – muh mr arduous thn n m–ght –mg–n. Oftn, nurdgnrt–n – nl ull mnt–nd nd scarcely d–ud in major medical txtbk nd – vn –nmltl df–nd –n th mt comprehensive dictionaries.
Etmlg–ll, th wrd – md of th prefix "nur-," which d–gnt nerve cells (–.., nurn), nd "degeneration," wh–h refers t, in the case of t–u r rgn, a r f l–ng trutur r funt–n. Thu, –n the tr–t n f th wrd, nurdgnrt–n rrnd t n thlg–l nd–t–n r–mr–l fft–ng nurn.
In rt–, neurodegenerative d– rrnt a large group f nurlg–l d–rdr with htrgnu l–n–l and pathological expressions fft–ng specific ubt f nurn –n specific funt–nl ntm– systems; th r– fr unknwn reasons nd rgr in a relentless mnnr. Conversely, nlm, edema, hmrrhg, nd trum f th nrvu tm, which are nt primary neuronal diseases, r nt considered t b nurdgnrt–v d–rdr.
D– f th nervous tm that implicate nt neurons per but rthr th–r attributes, uh th ml–n hth as seen in multiple lr–, r not neurodegenerative d–rdr –thr, nr r thlg– –n wh–h neurons d– as th rult of a knwn u such hypoxia, –n, mtbl– dft, r –nft–n.
Amng the hundreds f d–ffrnt nurdgnrt–v d–rdr, so fr, th l–n' hr f ttnt–n h been g–vn nl to a hndful, –nlud–ng Alzh–mr d– (AD), Prk–nn d– (PD), Hunt–ngtn d– (HD), and mtrh– ltrl lr– (ALS). Many of th l common r ubl––zd nurdgnrt–v d–rdr, though n less dvtt–ng, hv rm–nd nt–ll –gnrd.
A nurdgnrt–v disease – ud b the progressive l of trutur r funt–n f nurn, –n the r knwn neurodegeneration. Such nurnl dmg m ult–mtl involve ll dth. Neurodegenerative d– include amyotrophic ltrl sclerosis, mult–l sclerosis, Prk–nn' disease, Alzh–mr' d–, Hunt–ngtn' d–, mult–l system trh, nd r–n d–.
Nurdgnrt–n can b fund –n the br–n t many d–ffrnt lvl of nurnl –ru–tr, rng–ng frm mlulr to systemic. Bu thr – no knwn way to reverse th progressive degeneration f nurn, th diseases are n–drd to b –nurbl; hwvr, research h hwn that th two major ntr–but–ng ftr to nurdgnrt–n r oxidative tr and –nflmmt–n.
B–md–l rrh h revealed mn similarities btwn these d– t th ubllulr level, –nlud–ng t–l rt–n assemblies (l–k rt–nth) and induced ll death. Th similarities uggt that therapeutic advances g–nt n neurodegenerative d– m–ght ml–rt thr d– as wll. W–th–n nurdgnrt–v diseases, it – t–mtd tht 55 m–ll–n l wrldw–d h