neurodegenerative diseases

1. NEURODEGENERATIVE
DISEASES

2. CONTENTS
 Introduction
 Alzheimer’s disease
 Huntington’s disease
 Spinal Muscular Atrophy
 Conclusion
 References

3. INTRODUCTION
The word “Neurodegenerative”canbe splitinto “Neuro-”whichdesignatesnerve cellsi.e.,neurons,and
“degeneration,”whichrefersto,inthe case of tissuesororgans,a processof losingstructure orfunction.Thus,
neurodegeneration referstopathological conditionprimarilyaffectingneurons. Neurodegenerativediseases
representalarge groupof neurological disorderswithheterogeneousclinical andpathological expressionsaffecting
specificsubsetsof neuronsinspecificfunctionalanatomicsystems;theyarise forunknownreasonsandprogressina
relentlessmanner.
Amongthe hundredsof differentneurodegenerative disorders,so far, the lion’sshare of attentionhasbeengiven
onlyto a handful,includingAlzheimerdisease(AD),Parkinsondisease (PD),Huntingtondisease(HD),and
amyotrophiclateral sclerosis(ALS).Manyof the lesscommonorpublicizedneurodegenerativedisorders,thoughno
lessdevastating,have remainedessentiallyignored.
The most consistentriskfactorfordevelopinganeurodegenerative disorder,especiallyADorPD, isincreasingage.
Degenerativenerve diseasesaffectmanyof yourbody'sactivities,suchasbalance,movement,talking,breathing,
and heartfunction.Manyof these diseasesare genetic.Sometimesthe cause isamedical conditionsuchas
alcoholism,atumour,ora stroke.Othercausesmayinclude toxins,chemicals,andviruses.Sometimesthe cause is
unknown.
Degenerativenerve diseasesinclude
 Alzheimer's disease (AD)
 Huntington's disease(HD)
 Parkinson's disease(PD)
 Spinal muscularatrophy
Degenerativenerve diseasescanbe seriousorlife-threatening.Itdependsonthe type.Mostof themhave no cure.
Treatmentsmayhelpimprove symptoms,relieve pain,andincreasemobility.

4. ALZHEIMER’S DISEASE
Alzheimer'sdisease isaprogressive neurologicdisorderthatcausesthe brainto shrink(atrophy) andbraincellsto
die.Alzheimer'sdiseaseisthe mostcommoncause of dementia — a continuousdecline inthinking, behavioural and
social skillsthataffectsaperson'sabilitytofunctionindependently.
Approximately5.8millionpeople inthe UnitedStatesage 65 and olderlive withAlzheimer'sdisease.Of those,80%
are 75 yearsoldand older.Outof the approximately50millionpeople worldwidewithdementia,between60%and
70% are estimatedtohave Alzheimer'sdisease.
Causes
The exact causesof Alzheimer'sdiseasearen'tfullyunderstood.Butata basiclevel,brainproteinsfail tofunction
normally,whichdisruptsthe workof braincells(neurons) andtriggersaseriesof toxicevents.Neuronsare
damaged,lose connectionstoeachotherand eventuallydie.
Scientistsbelieve thatAlzheimer'sdiseaseiscausedbya combinationof genetic,lifestyleandenvironmental factors
that affectthe brainovertime.
Lessthan 1% of the time,Alzheimer'siscausedbyspecificgeneticchangesthatvirtuallyguaranteeapersonwill
developthe disease.These rare occurrencesusuallyresultindisease onsetinmiddleage.
The damage most oftenstartsin the regionof the brainthat controlsmemory,butthe processbeginsyearsbefore
the firstsymptoms.The lossof neuronsspreadsina somewhatpredictable patterntootherregionsof the brains.By
the late stage of the disease,the brainhasshrunksignificantly.
Researcherstryingtounderstandthe cause of Alzheimer'sdisease are focusedonthe role of twoproteins:
Plaques Beta-amyloidisafragmentof a largerprotein.Whenthese fragmentsclustertogether,theyappeartohave
a toxiceffectonneuronsandto disruptcell-to-cell communication.These clustersformlargerdepositscalled
amyloidplaques,whichalsoinclude othercellulardebris.
Tangles Tauproteinsplayapartin a neuron'sinternal supportandtransportsystemtocarry nutrientsandother
essential materials.InAlzheimer'sdisease,tauproteinschange shape andorganize themselvesintostructurescalled
neurofibrillarytangles.The tanglesdisruptthe transportsystemandare toxictocells.

5. Pathophysiology
Alzheimerdisease core neuropathologicfindingsincludeextracellularamyloidplaques,intracellularNFTs,synaptic
deterioration,andneuronal death. Granulovacuolardegenerationinthe hippocampusandamyloiddepositionin
bloodvessels(congophilicangiopathy) mayalsobe seenontissue examination,butare notrequiredforthe
diagnosis.The "amyloidcascade"hypothesispositsthatamyloidplaquesinterfere withsynapticactivityandinitiate
a seriesof downstreameffectsthatcause increasinginter-andintraneuronaldysfunctionand,ultimately,cell death.
Amyloid Plaques
Althoughamyloidplaquesmaybe subclassifiedaccordingtotheircomposition,all containformsof β-amyloid
protein(Aβ).Aβisanaminoacid peptide formedbyproteolyticcleavage of APPbyβ- andγ-secretase.The main
productsof thiscleavage are Aβ1–40 and Aβ1–42. A relative surplusof Aβ1–42 predisposestowardamyloid
aggregationintooligomersandfibrils,whichassemble intoamyloidplaques.Animportantrole foramyloidin
Alzheimerpathophysiologyisimpliedbythe factthatthe proteinsencodedbyAPP,PS1,PS2,SorL1, andApoE are all
associatedwithamyloidgeneration,processing,ortrafficking.However,several linesof evidenceindicatethat
amyloidplaquesare notthe primarycause of Alzheimer.
Amyloidplaqueburden
 can be foundincognitivelynormal adults,
 doesnotcorrelate withdegree of cognitive impairmentinindividualswithADdementia.
NeurofibrillaryTangles
Tau, a proteininvolvedinmicrotubule assembly, isessential fornormal axonal growthandneuronal development.
However,hyperphosphorylatedtauproteinaggregatesintohelical filamentousNFTthatare depositedpreferentially
withinneuronsof the mesial temporal lobe(especiallyhippocampus),lateral parietotemporal region,andthe frontal
associationcortices.The critical role of NFTinAlzheimerpathophysiologyissuggestedbythe correlationbetween
locationanddensityof tauNFT and the symptomsandseverityof Alzheimerdementia. Moreover,some studies
have demonstratedthatAβoligomersare nottoxicunlesstauisalsopresent.
Neuron and Synapse Loss
The distributionof neuronal celldeathandsynapse lossissimilartothatof NFT. In typical Alzheimer,the deathof
neuronsinthe nucleusbasalisof Meynertleadstoadeficitinacetylcholine (Ach),aneurotransmitterinvolvedin
memory.Thischolinergicdeficitisthe targetof most currenttreatments.Inthe brainstem, lossof medianraphe and
locuscoeruleus neuronsleadstodeficitsinserotoninandnorepinephrine,respectively.Abnormalcerebral
serotonergicandadrenergicactivitylikelycontribute todysphoriaandinsomniainAlzheimer.

6. Symptoms
Memorylossis the keysymptomof Alzheimer'sdisease.Earlysignsinclude difficulty rememberingrecenteventsor
conversations.Asthe diseaseprogresses,memoryimpairmentsworsenandothersymptomsdevelop.A personwith
Alzheimer'sdisease maybe aware of havingdifficultyrememberingthingsandorganizingthoughts. Brainchanges
associatedwithAlzheimer'sdisease ledtogrowingtroublewith:
Memory
Everyone hasoccasional memorylapses,butthe memorylossassociatedwithAlzheimer'sdisease persistsand
worsens,affectingthe abilitytofunctionatworkor at home.
People with Alzheimer'smay:
 Repeatstatementsandquestionsoverandover
 Forgetconversations,appointmentsorevents,andnotrememberthemlater
 Routinelymisplace possessions,oftenputtingtheminillogicallocations
 Get lostinfamiliarplaces
 Eventuallyforget the namesof familymembersandeverydayobjects
 Have trouble findingthe rightwordstoidentifyobjects,expressthoughtsortake partin conversations
Thinking and reasoning
Alzheimer'sdisease causesdifficultyconcentratingandthinking,especiallyaboutabstractconceptssuchas numbers.
Multitaskingisespeciallydifficult,anditmaybe challengingtomanage finances,balance checkbooks andpaybills
on time.Eventually,apersonwithAlzheimer'smaybe unable torecognize anddeal withnumbers.
Making judgments and decisions
Alzheimer'scausesadecline inthe abilitytomake reasonable decisionsandjudgmentsineverydaysituations.For
example,apersonmaymake pooror uncharacteristicchoicesinsocial interactionsorwearclothesthatare
inappropriate forthe weather.Itmaybe more difficulttorespondeffectivelytoeverydayproblems,suchasfood
burningonthe stove orunexpecteddrivingsituations.
Planning and performing familiar tasks
Once-routine activitiesthatrequire sequential steps,suchasplanningandcookinga meal or playinga favourite
game,become a struggle asthe disease progresses.Eventually,peoplewithadvancedAlzheimer'softenforgethow
to performbasictaskssuch as dressingandbathing.

7. Changes in personalityand behaviour
Brain changesthatoccur inAlzheimer'sdisease canaffectmoodsand behaviours.Problemsmayinclude the
following:
 Depression
 Apathy
 Social withdrawal
 Mood swings
 Distrustinothers
 Irritabilityandaggressiveness
 Changesinsleepinghabits
 Wandering
 Loss of inhibitions
 Delusions,suchasbelievingsomethinghasbeenstolen
 Preservedskills
Many importantskillsare preservedforlongerperiodsevenwhilesymptomsworsen.Preservedskillsmayinclude
readingor listeningtobooks,telling storiesandreminiscing,singing,listeningtomusic,dancing,drawing,ordoing
crafts. These skillsmaybe preservedlongerbecause theyare controlledbypartsof the brainaffectedlaterinthe
course of the disease.
Complications
Memoryand language loss,impairedjudgmentandothercognitive changescausedbyAlzheimer'scancomplicate
treatmentforotherhealthconditions.A personwithAlzheimer'sdisease maynotbe able to:
 Communicate thathe or she isexperiencingpain
 Explainsymptomsof anotherillness
 Followaprescribedtreatmentplan
 Explainmedicationside effects
As Alzheimer'sdisease progressestoitslaststages,brainchangesbegintoaffectphysical functions,suchas
swallowing,balance,andbowelandbladdercontrol.
Prevention
Alzheimer'sdisease isnotapreventable condition.However,anumberof lifestyleriskfactorsforAlzheimer'scanbe
modified.Evidence suggeststhatchangesindiet,exercise andhabitsmayloweryourriskof developingAlzheimer's
disease andotherdisordersthatcause dementia.Healthylifestyle choicesthatmayreduce the riskof Alzheimer's
include the following:
 Exercisingregularly
 Eatinga dietof freshproduce,healthyoilsandfoodslow insaturatedfatsuch as a Mediterraneandiet
Studieshave shownthatpreservedthinkingskillslaterinlife andareducedriskof Alzheimer'sdiseaseare associated
withparticipatinginsocial events,reading,dancing,playingboardgames,creatingart,playinganinstrument,and
otheractivitiesthatrequire mentalandsocial engagement.

8. HUNTINGTON’S DISEASE
Huntington'sdisease isarare,inheriteddiseasethatcausesthe progressivebreakdown(degeneration) of nervecells
inthe brain.Huntington'sdiseasehasabroad impacton a person'sfunctional abilitiesandusuallyresultsin
movement,thinking(cognitive) andpsychiatricdisorders.
Huntington'sdisease symptomscandevelopatanytime,buttheyoftenfirstappearwhenpeople are intheir30sor
40s. If the conditiondevelopsbefore age 20,it's calledjuvenileHuntington'sdisease.WhenHuntington'sdevelops
early,symptomsare somewhatdifferentandthe disease mayprogressfaster.
Causes
Autosomal dominantinheritance
Huntington'sdisease iscausedbyaninheriteddefectina single gene. Huntington'sdiseaseisanautosomal
dominantdisorder,whichmeansthatapersonneedsonlyone copyof the defectivegene todevelopthe disorder.
Withthe exceptionof genesonthe sex chromosomes,apersoninheritstwocopiesof everygene — one copyfrom
each parent.A parentwitha defective genecouldpassalongthe defective copyof the gene orthe healthycopy.
Each childinthe family,therefore,hasa50% chance of inheritingthe gene thatcausesthe geneticdisorder.

9. Pathophysiology
In Huntingtondisease,the caudate nucleusatrophies,the inhibitorymediumspinyneuronsinthe corpusstriatum
degenerate,andlevelsof the neurotransmittersgamma-aminobutyricacid(GABA) andsubstance Pdecrease.
Huntingtondisease resultsfromamutationinthe huntingtin (HTT) gene (onchromosome4),causingabnormal
repetitionof the DNA sequence CAG,whichcodesforthe aminoacidglutamine.The resultinggeneproduct,alarge
proteincalledhuntingtin,hasanexpandedstretchof polyglutamine residues,which accumulatewithinneuronsand
leadto disease viaunknownmechanisms.The more CAGrepeats,the earlierthe onsetof disease andthe more
severe itsexpression(phenotype).The numberof CAGrepeatscanincrease withsuccessivegenerationswhenthe
fathertransmitsthe mutationand,overtime,canleadto increasinglyseverephenotypeswithinafamily(called
anticipation).
Symptoms and Signs
Symptomsandsignsof Huntingtondisease developinsidiously,startingataboutage 35 to 40, dependingon
phenotype severity.
Huntington'sdisease usuallycausesmovement,cognitive andpsychiatricdisorderswithawide spectrumof signs
and symptoms.Whichsymptomsappearfirstvariesgreatlyfrompersontoperson.Some symptomsappearmore
dominantorhave a greatereffectonfunctional ability,butthatcan change throughoutthe course of the disease.
Movementdisorders
The movementdisordersassociatedwithHuntington'sdiseasecaninclude bothinvoluntarymovementproblems
and impairmentsinvoluntarymovements,suchas:
 Involuntaryjerkingorwrithingmovements(chorea)
 Muscle problems,suchasrigidityormuscle contracture (dystonia)
 Slowor abnormal eye movements
 Impairedgait,posture andbalance
 Difficultywithspeechorswallowing

10. Impairmentsinvoluntarymovements — ratherthanthe involuntarymovements — mayhave a greaterimpacton a
person'sabilitytowork,performdailyactivities,communicate andremainindependent.
Cognitive disorders
Cognitive impairmentsoftenassociatedwithHuntington'sdisease include:
 Difficultyorganizing,prioritizingorfocusingontasks
 Lack of flexibilityorthe tendencytogetstuck ona thought,behaviororaction(perseveration)
 Lack of impulse control thatcanresultinoutbursts,actingwithoutthinkingand sexualpromiscuity
 Lack of awarenessof one'sownbehaviorsandabilities
 Slownessinprocessingthoughtsor''finding''words
 Difficultyinlearningnewinformation
Psychiatric disorders
The most commonpsychiatricdisorderassociatedwithHuntington'sdisease isdepression.Depressionappearsto
occur because of injurytothe brainand subsequentchangesinbrainfunction.Signsandsymptomsmayinclude:
 Feelingsof irritability,sadnessorapathy
 Social withdrawal
 Insomnia
 Fatigue andlossof energy
 Frequentthoughtsof death,dyingorsuicide
Othercommonpsychiatricdisordersinclude:
Obsessive-compulsive disorder, aconditionmarkedbyrecurrent,intrusive thoughtsandrepetitive behaviours
Mania, whichcan cause elevatedmood,overactivity,impulsive behaviourandinflatedself-esteem
Bipolar disorder, a conditionwithalternatingepisodesof depressionandmania
Weightlossiscommoninpeople withHuntington'sdisease,especiallyasthe disease progresses.

11. Symptoms of juvenile Huntington's disease
The start andprogressionof Huntington'sdisease inyoungerpeoplemaybe slightlydifferentfromthatinadults.
Problemsthatoftenpresentearlyinthe course of the disease include:
 Behavioral changes
 Difficultypayingattention
 Rapid,significantdropinoverall school performance
 Behavioral problems
 Physical changes
 Contractedand rigidmusclesthataffectgait(especiallyinyoungchildren)
 Tremorsor slightinvoluntarymovements
 Frequentfallsorclumsiness
 Seizures
Complications
AfterHuntington's diseasestarts,aperson'sfunctional abilitiesgraduallyworsenovertime.The rate of disease
progressionanddurationvaries.
The clinical depressionassociatedwithHuntington'sdisease mayincreasethe riskof suicide.Some researchsuggests
that the greaterriskof suicide occursbefore adiagnosisismade andinthe middle stagesof the disease whena
personstartsto lose independence.
Eventually,apersonwithHuntington'sdiseaserequireshelpwithall activitiesof dailylivingandcare.Late in the
disease,he orshe will likelybe confinedtoabedand unable tospeak.Someone withHuntington'sdiseaseis
generallyable tounderstandlanguage andhasan awarenessof familyandfriends,thoughsome won'trecognize
familymembers.
Commoncausesof deathinclude:
 Pneumoniaorotherinfections
 Injuriesrelatedtofalls
 Complicationsrelatedtothe inabilitytoswallow
Prevention
Huntington’sdisease cannotbe actuallyprevented.Forpeople carryingmutatedgenesthere isa50% chance to
have a child withthisdisease.Because of that,doctorsadvise counsellingforeveryonewhohasa close family
membersufferingfromHuntington’s.Genetic counsellingandbloodtestscouldhelpthese peopletodetermine the
presence of mutatedgene responsible forthisdisease yearsbefore itshowsanysymptoms.
Parentcarriersof the gene forHuntington’sdiseasecouldbe advisedtothinkaboutassistedreproductionand
screeningthe embryosforgene mutation.Anotheroptionforthese parentsmaybe adoption.
Huntington’sdisease canbe treatedwithmedicationsinordertomanage the symptomsandmake life easierfor
these patients.However,the diseaseisprogressive andthere isnotreatmentavailable topreventanyphysical or
mental problemrelatedtothismedical condition.Patientsare advisedtoexerciseregularly,becausephysical activity
has proventobe helpful inmanagingthe condition.Make sure towear propershoesduringthese activities,to
enhance yourstabilityandyouwill ensurebothmental andphysical benefitsof exercise.

12. SPINAL MUSCULAR ATROPHY
Spinal muscular atrophy 1 (SMA1),alsoknownas WerdnigHoffmanndisease,isagenetic neuromuscular
disorderthataffectsthe nerve cellsthatcontrol voluntarymuscles(motorneurons). Musculardystrophyisagroup
of diseasesthatcause progressive weaknessandlossof muscle mass.Inmusculardystrophy,abnormal genes
(mutations) interfere withthe productionof proteinsneededtoformhealthymuscle.
Causes
The most commonformof SMA iscausedby defectsinbothcopiesof the survival motorneuron1 gene (SMN1) on
chromosome 5q.Thisgene producesthe survival motor neuron(SMN) proteinwhichmaintainsthe healthand
normal functionof motorneurons.IndividualswithSMA have insufficientlevelsof the SMN protein,whichleadsto
lossof motor neuronsinthe spinal cord,producingweaknessandwastingof the skeletal muscles. Thisweaknessis
oftenmore severe inthe trunkandupperlegand arm musclesthaninmusclesof the handsand feet.
There are manytypesof spinal muscularatrophythatare causedby changesinthe same genes. Lesscommonforms
of SMA are caused by mutationsinothergenesincludingthe VAPBgene locatedonchromosome 20,the DYNC1H1
gene onchromosome 14, the BICD2 gene onchromosome 9,and the UBA1 gene onthe X chromosome. The types
differinage of onsetand severityof muscle weakness;however,there isoverlapbetweenthe types.

13. Pathophysiology
The most commonformof SMA (types1-4) is causedbya defect - mutationinthe SMN1gene onchromosome5.
(People have two SMN1genes — one oneachchromosome 5).In 94% of all SMA cases,thismutationinvolvesa
deletioninasegmentknownasexon7.Thisarea islocatedinthe longarm of the chromosome 5,in the 5q13.2
region. A mutationinthe SMN1gene leadstoa deficiencyof amotor neuronproteincalled SMN,whichstands
for “survivalof motorneuron.”Asitsname implies,thisproteinisresponsible forgene expressionnecessaryfor
normal motor neuronfunction.
More rarely,a mutationinan X-chromosome genecalled UBE1causes X-linked SMA.The UBE1 gene carries
instructionsforubiquitin-activatingenzyme1,whichnormallyhelpsattachamoleculartagto proteinstomark them
for destruction.
Flawsinthe cytoplasmicdynein 1 heavy chain 1 (DYNC1H1) gene onchromosome 14 have beenfoundtoleadto
anotherrare formof SMA called SMA-LED.
Symptoms
The main signof musculardystrophyisprogressive muscle weakness.Specificsignsandsymptomsbeginatdifferent
agesand indifferentmuscle groups,dependingonthe type of musculardystrophy.
Duchenne type muscular dystrophy
Thisis the mostcommon form.Althoughgirlscanbe carriersand mildlyaffected,it'smuchmore commonin boys.
Signsand symptoms,whichtypicallyappearinearlychildhood,mightinclude:
 Frequentfalls
 Difficultyrisingfromalyingor sittingposition
 Trouble runningandjumping
 Waddlinggait
 Walkingonthe toes
 Large calf muscles
 Muscle painand stiffness
 Learningdisabilities
 Delayedgrowth
Becker muscular dystrophy

14. Signsand symptomsare similartothose of Duchenne musculardystrophy,buttendto be milderandprogressmore
slowly.Symptomsgenerallybegininthe teensbutmightnotoccuruntil the mid-20sor later.
Other typesof muscular dystrophy
Some typesof musculardystrophyare definedbyaspecificfeature orbywhere inthe bodysymptoms begin.
Examplesinclude:
Myotonic Thisischaracterizedbyan inabilitytorelax musclesfollowingcontractions.Facial andneckmusclesare
usuallythe firsttobe affected.People withthisformhave long,thinfaces;droopingeyelids;andswanlike necks.
Facioscapulohumeral (FSHD) Muscle weaknesstypicallybeginsinthe face,hipandshoulders.The shoulderblades
mightstickout like wingswhenarmsare raised.Onsetusuallyoccursinthe teenage yearsbutcan begininchildhood
or as late as age 50.
Congenital Thistype affectsboysandgirlsand isapparentat birthor before age 2. Some formsprogressslowlyand
cause onlymilddisability,whileothersprogressrapidlyandcause severe impairment.
Limb-girdle Hipandshouldermusclesare usuallyaffectedfirst.People withmusculardystrophymighthave difficulty
liftingthe frontpartof the footand so mighttripfrequently.Onsetbeginsinchildhoodorthe teenage years.
Complications
The complicationsof progressivemuscleweaknessinclude:
 Trouble walking. Some people withmusculardystrophyeventuallyneedtouse awheelchair.
 Trouble using arms. Dailyactivitiescanbecome more difficultif the musclesof the armsand shouldersare
affected.
 Shorteningof musclesor tendonsaround joints (contractures).Contracturescan furtherlimitmobility.
 Breathing problems. Progressive weaknesscanaffectthe musclesassociatedwithbreathing.Peoplewith
musculardystrophymighteventuallyneedtouse abreathingassistance device (ventilator),initiallyatnight
but possiblyalsoduringthe day.
 Curvedspine (scoliosis). Weakenedmusclesmightbe unable toholdthe spine straight.
 Heart problems.Musculardystrophycan reduce the efficiencyof the heartmuscle.
 Swallowingproblems. If the musclesinvolvedwithswallowingare affected,nutritional problemsand
aspirationpneumoniacandevelop.Feedingtubesmightbe anoption.
Prevention
Doctor islikelytostart witha medical historyandphysical examination. Afterthat,doctormightrecommend:
 Enzyme tests Damagedmusclesrelease enzymes,suchascreatine kinase (CK),intoyourblood.Inaperson
whohasn't had a traumaticinjury,highbloodlevelsof CKsuggestamuscle disease.
 GenetictestingBloodsamplescanbe examinedformutationsinsome genesthatcause typesof muscular
dystrophy.
 Muscle biopsyA small piece of muscle canbe removedthroughanincisionorwitha hollow needle.Analysis
of the tissue sample candistinguishmusculardystrophiesfromothermuscle diseases.
 Heart-monitoringtests (electrocardiographyand echocardiogram) These testsare usedto checkheart
function,especiallyinpeople diagnosedwithmyotonicmusculardystrophy.
 Lung-monitoringtestsThese testsare usedto check lungfunction.
 Electromyography. Anelectrode needleisinsertedintothe muscle tobe tested.Electrical activityis
measuredasyourelax and as yougentlytightenthe muscle.Changesinthe patternof electrical activitycan
confirma muscle disease.

15. CONCLUSION
Peopleall overthe world are suffering fromneurodegenerativediseases,which areillnessesthat lead to cell deathin
the brain. Neurodegenerativediseases,likeHuntington’sDisease,affectthebasalganglia and lead to movement
difficulties.Other diseasescausemorewidespread cell death and lead to memory loss,which is seen in Alzheimer’s
Disease and Lewy body dementia.Thereare also rarer typesof neurodegenerativediseasesthatwerenotcovered in
this article. Neurodegenerativediseasesarehorribleillnesses to have,and thereis currently no cure; however,
researchersaround theworld are looking into waysto help peoplewith thesediseases.Oneof themost exciting
treatmentsusesstemcells to replace the neuronsthathavedied.
The effectof Alzheimer’sdiseaseon several body systems, analysed theimpactsof genetics,gender,ethnicity,age,
and behaviouron pathophysiology of thedisease,and identified effectivemethodsof treatmentof Alzheimer’s
disease,it is possibleto inferthat this progressiveneurodegenerativeillnessnegatively impactscentralnervous
systemaswell as neuromuscularand respiratoryfunctionsof a human body.Themostcommon symptomsof
Alzheimer’sdiseaseare increased confusion,disorientation,mood swings,problemswith reading,talking,and
writing,significantdifficulties while performing spatialtasks,and seriousproblemswith short-termaswellas long-
term memory.Genetics,gender,ethnicity,lifestyle, age,and behaviourinfluencethedevelopmentand progressionof
the disease.Despite thefact thatthere is no effectivecure forAlzheimer’sdisease,healthy lifestyle, physical
exercising,balanced diet,caregiving,numerouspsychologicalinterventions,and traditionalmedicationsmay
increase thequality of life of patientswithAlzheimer’sdiseaseand their longevity.
Huntington'sDiseaseis one of the worstgenetic disordersthatonecan have.Ithasa wide array of negativeeffects,
is currently incurable,and inevitably resultsin death.However,there is hopefor thefuture,asmany scientists are
working on waysto combatthis disorder.
Spinal MuscularAtrophyis a rare disease thathasdevastating effectson theneuromuscularsystemresulting in
progressiveweakness.Thisdiseaseoften leadsto shortened lifespan dueto progressiverespiratory failure,especially
in the mostsevere subtypes.
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