Cure of Amyotropic Sclerosis

Cure of Amyotropic Sclerosis
Kunal Joon *


*Correspondence to: Kunal Joon, Noida International Institute of Medical Sciences.


© 2024 Kunal Joon. 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.

Received: 12 April 2024

Published: 25 April 2024


It is neurodegenerative disorder affecting primary motor system but in which extra motor manifestation are increasingly recognized .ALS often has a focal onset but subsequently spreads to different body regions, where failure of respiratory muscles typically limits survival to 2–5 years after disease onset. In up to 50% of cases, there are extra?motor manifestations such as changes in behaviour, executive dysfunction and language problems. In 10%–15% of patients, these problems are severe enough to meet the clinical criteria of frontotemporal dementia (FTD).

Keywords: Amyotrophic lateral sclerosis, sporadic and familial ALS, TDP?43 pathology.

Cure of Amyotropic Sclerosis


Figure 1

Grouping  of ALS  genes in pathologic pathways . (1) Mutations in TBK?1, OPTN, SQSTM1 (= p62), UBQLN2, C9orf72 and VCP affect the protein[1] degradation  of pathways and may contribute to TDP?43 accumulation. (2) Mutations in TARDBP, FUS, MATR3, TIA1, hnRNPA1, hnRNA2B1 and[2] ATXN2 gene  may all affect RNA metabolism. (3) Mutations in TUBA4A, PFN1, KIF5A and DCTN1 alteration of  cytoskeletal dynamics and axonal transport.[3]



Neuropathological signof ALS is characterized by loss of the neuromuscular connection, axonal retraction and subsequent cell death of UMNs ( upper motor neurons ) and LMNs(lower motor neurons ), surrounded by astrogliosis[4] and microgliosis, with ubiquitin?positive inclusions being observed in surviving neurons.[5] TDP?43 is  main component of these inclusions in more than 95% of ALS[6] patients . TDP?43 is an RNA? and DNA?binding protein involved in multiple processes such as transcription, splicing, micro RNA maturation, RNA transport and stress granule formation. In[7] line with its nuclear and cytoplasmic functions, TDP?43 can shuttle between the nucleus and the cytoplasm, but its localization is mainly nuclear. Unlocalization  to the[8] cytoplasm, leading to nuclear depletion of TDP?43 along with cytoplasmic protein aggregation,[9] is a hallmark of ALS.


Clinical presentation

Figure 2

It shows the phenotypic  representation of the Amyotropic sclerosis [10]

Cure of Amyotropic sclerosis


Stemcell brain therapy

Implantation of the progenitors  neurons lead to development  of  the neurons and affected  neurons can be replaced  by new neurons through stem cell brain therapy and lead to development  and cure of the Amyotropic sclerosis

Dose 1) stem cell neuron progenitors  cell injected through spinal needle through cervical puncture

Dose 2) Nutritional dose which gives nutrition  to the cell

Dose 3) monoclonal  antibodies  against the deformed or degenerated neurons .



1.) Aetiology of Amyotropic sclerosis

2.)clinical feature of Amyotropic sclerosis

3.) Cure of Amyotropic sclerosis



Cure of Amyotropic sclerosis is found and pathogenesis and aetiological studies of Amyotropic sclerosis.













Figure 1

Figure 2

slot gacor mudah maxwinagen judi bola resmimahjong ways pola jitu maxwinpola gacor starlight princessslot server kambojarahasia scatter hitam mahjong waysturbo spin slot mahjongrtp slot candy villagepola gacor mahjong wins terbaruslot server luar terbarurtp slot olympusslot mahjong waysrtp sweet bonanzaagen sbobet euro 2024judi bola parlay sbobetslot gates of olympus jepe maxwinrtp slot gacorslot starlight christmas pragmaticslot server filipinaslot deposit danaslot mahjong wins banjir scatterpola gacor mahjong maxwinjackpot naga hitam slot mahjong winsrumus slot mahjongrahasia scatter hitam slot mahjongdemo mahjong mudah menangrtp pg softrumus sbobet mix parlay