





































Abstract

Berkeley
Pharma Tech
Journal of Medicine

Correspondence:
ashleyvaratip@gmail.com

Keywords:
stimulants, non-stimulants, 
neurotransmission, 
Neurexins 1 (NRXN1), 
Dopamine receptor D3 (DRD3), 
Glutamic Acid Decarboxylase 65 
(GAD65), Patched Domain 
Containing 1 gene (Ptchd1), 
Norepinephrine Transporter 
(SLC6A2)

Submitted: January 20, 2023 
Accepted: February 9, 2023 
Published: June 30, 2023

Full Open Access

Creative Commons Attribution 
License 4.0

Issues regarding disorganization and hyperactivity are large burdens on 
the pediatric population, and the severity of these behavioral disorders, 
called attention-deficit hyperactivity disorder (ADHD), falls on the 
slow-developing treatments that are unable to fully solve the symptoms of 
those affected. Limiting factors include the heterogeneous responses that 
many patients have in response to pharmacological treatments, the range 
of comorbid symptoms and conditions associated with ADHD, and the 
intricacies of the environmental and genetic interactions involved. Since 
ADHD has a strong genetic component with up to 80% heritability for the 
condition, epigenetic and genetic studies offer valuable insight into how 
future treatments could tackle the issue. In particular, the studies reveal 
how genes might provide indicators for patients’ response to medication, 
their symptomatology, and unique risks for comorbidities. This paper 
outlines the current pharmacological and cognitive treatments for ADHD, 
discusses their limitations, and offers an overview of present genetic risk 
factors to analyze how they may provide insights for detection, prevention, 
and responses to treatment.

By: Ashley Varatip, Serena Z. H. Huang, Yash Kilam, Cameron Asadi

The Predictive Power of Attention-Deficit 
Hyperactivity Disorder (ADHD) Genetic 
Risk Factors



 Introduction 

 1.1  Introduction to ADHD 

 Attention-de�cit  hyperactivity  disorder  (ADHD)  primarily  a�ects  children 
 and  adolescents.  As  of  2016,  there  are  6.1  million  (9.4%)  children  aged  2-17 
 diagnosed  with  ADHD  in  the  United  States  1  .  Along  with  that,  1  in  20 
 children  in  the  United  States  are  being  medicated  for  ADHD  1  .  While 
 present  in  younger  populations,  it  can  persist  into  adulthood  as  well. 
 2.5-4.4%  of  adults  in  the  United  States  are  diagnosed  with  ADHD  and 
 around  2.8%  of  adults  worldwide  2  .  The  main  characteristic  behaviors 
 de�ned  by  this  disorder  can  include  hyperactivity,  short  attention  span,  and 
 impulsiveness.  Children  and  adults  can  display  these  symptoms  di�erently. 
 Hyperactivity  and  impulsiveness  tend  to  be  traits  shown  more  in  children 
 while  inattentiveness  is  more  persistent  in  adults  3  .  For  example,  children  can 
 exhibit  hyperactivity  by  not  being  able  to  sit  still.  Adults  on  the  other  hand 
 can  show  signs  of  inattention  by  not  being  able  to  sit  through  long  activities 
 or interrupting people’s sentences while they talk. 

 1.2  Causes of ADHD 

 The causes and the risk factors of ADHD are unknown to this day. 
 However, it is believed that genetics plays a very important role in the 
 development of ADHD in individuals  4  . ADHD tends to  run in the family, 
 transmitted through genes inherited from one’s parents  5  .  Recent analysis of 
 twin studies demonstrates 80% heritability for the condition, though no 
 speci�c genes have been linked to ADHD  6  . Along with  genetics, some risk 
 factors include brain injury, exposure to environmental risks during 
 pregnancy or at a young age, alcohol or tobacco use during pregnancy, 
 premature delivery, or low birth weight  4  . 

 1.3  Diagnosis of ADHD 

 Currently,  there  are  no  convenient  or  de�nitive  ways  to  diagnose  ADHD. 
 Children  can  get  diagnosed  with  ADHD  by  a  pediatrician,  adult 
 psychiatrist,  or  quali�ed  healthcare  professional  with  training  in  ADHD  7  .  A 
 physical  examination  is  run  to  make  sure  the  symptoms  relayed  are  not 
 caused  by  something  other  than  ADHD.  Then,  an  interview  can  be 

 Berkeley Pharma Tech Journal of Medicine |  60 



 conducted  with  the  child  and  parent.  To  be  diagnosed  with  ADHD, 
 multiple  symptoms  must  be  displayed.  Additionally,  the  patient  must 
 experience  these  symptoms  for  over  six  months  and  before  the  age  of 
 twelve  7  .  This  process  can  be  di�erent  for  adults,  though  specialists  will  ask 
 the  adult  about  symptoms  that  they  have.  However,  an  adult  will  not  get  a 
 con�rmed  diagnosis  unless  they  a�rm  that  symptoms  were  present  in 
 childhood  7  .  All  of  these  diagnostic  tests  mainly  involve  speaking  to  a 
 specialist or doctor because no blood or invasive tests can diagnose ADHD  8  . 

 1.4  Current Treatments 

 The  most  popular  treatments  of  ADHD  include  the  use  of  medical 
 stimulants  or  non-stimulants.  Medical  stimulants  aim  to  correct 
 biochemical  imbalances  by  increasing  dopamine  and  norepinephrine  levels 
 to  increase  attention  and  focus  9  .  Stimulants  target  the  brain’s  reward 
 system,  the  mesolimbic  dopamine  pathway  involving  the  ventral  tegmental 
 area  of  the  midbrain,  medial  prefrontal  cortex,  and  limbic  system  10  .  In 
 general,  stimulant  medications  have  three  functions.  It  could  mimic 
 neurotransmitters  such  as  dopamine  to  increase  stimulation  of  dopamine 
 receptors.  It  could  increase  the  time  in  which  dopamine  stays  within  the 
 receptors  by  preventing  its  degradation.  This  could  occur  through  blocking 
 reabsorption  or  enzymatic  degradation  10  .  The  FDA  was  able  to  approve  29 
 medical  stimulants  including  Adderall,  Dexedrine,  and  Ritalin,  and  all 
 twenty-nine  of  these  stimulants  have  something  in  common:  the  use  of 
 either  the  molecule  amphetamine  or  methylphenidate  9  .  This  is  a  popular 
 choice  of  medication  for  ADHD  because  it  is  proven  to  help  around 
 70-80% of children with the diagnosis  9  .

 Although  stimulants  provide  good  results  for  most  pediatric  patients,  there 
 are  some  downsides  of  using  them.  The  side  e�ects  of  these  stimulants 
 include  an  increased  heart  rate,  increased  blood  pressure,  decreased  appetite, 
 anxiety,  and  a  chance  of  addiction  to  medications  9  .  Along  with  that, 
 stimulants  are  not  a  good  long-term  treatment  for  ADHD.  The  need  for 
 each  dose  of  the  stimulant  increases  over  time  and  it  was  found  that 
 stimulants may have less e�cacy over time  9  . 

 Since  there  are  downsides  to  using  stimulants,  non-stimulant  medications 
 are  a  relatively  new  medical  option  that  was  created  to  reduce  the  likelihood 

 Berkeley Pharma Tech Journal of Medicine |  61 



 for  drug  misuse  9  .  Non-stimulants  and  stimulants  are  very  similar  with  the 
 main  di�erence  being  the  target  neurotransmitter.  Strattera  (Atomoxetine) 
 was  the  �rst  FDA  approved  non-stimulant  medication  for  ADHD  with 
 Clonidine,  Guanfacine,  and  Qelbree  following  not  soon  after  9  . 
 Non-stimulants  have  fewer  side  e�ects,  but  side  e�ects  like  nervousness, 
 sleep  problems,  fatigue,  upset  stomach,  dizziness,  or  a  dry  mouth  can  still 
 happen  9  .  Although  it  seems  like  non-stimulants  are  a  good  option  of 
 treatment,  it  can  be  less  reliable  as  20-30%  of  people  with  ADHD  have 
 stated that it does not work for them  9  . 

 Another  option  for  treatment  for  ADHD  is  cognitive  behavioral  therapy, 
 also  known  as  CBT.  CBT  is  a  short-term  psychotherapy  that  focuses  on 
 changing  a  person’s  negative  perspective  of  themselves  11  .  This  could  mean 
 changing  the  way  one  thinks  about  themself  and  their  potential.  The  way 
 CBT  works  is  that  each  session  identi�es  situations  where  a  lack  of 
 organization  creates  problems  in  a  person’s  everyday  life  11  .  Therefore,  these 
 sessions  help  the  person  develop  coping  skills  to  deal  with  challenges  and 
 obligations.  These  sessions  can  also  include  time  for  relaxation  and 
 meditation  as  well.  There  is  a  recent  study  that  shows  the  positive  e�ect  of 
 CBT  through  a  randomized  controlled  trial  12  .  The  study  primarily  focused 
 on  determining  how  a  treatment  called  Accessing  Campus  Connections 
 and  Empowering  Student  Success  (ACCESS),  a  CBT  program,  a�ects  250 
 college  students  with  ADHD  over  a  course  of  two  semesters.  The  study 
 assessed  primary  characteristics  associated  with  ADHD  such  as  executive 
 functioning,  depression,  and  anxiety.  The  results  of  the  study  show  that 
 CBT  reduced  these  common  ADHD  symptoms.  Furthermore,  a  learning 
 curve  growth  of  students  was  modeled  and  it  showed  improvements 
 compared  to  groups  not  in  the  ACCESS  participants.  There  were  no 
 ascertained  changes  seen  in  depression  and  anxiety  with  correlations  for 
 lower  chances  in  worsening  depression  and  anxiety  symptoms.  Therefore,  it 
 provides  concrete  evidence  for  ACCESS  being  used  as  treatment  for  college 
 students with ADHD  12  . 

 Berkeley Pharma Tech Journal of Medicine |  62 



 Genes of Interest 

 As  discussed  earlier,  genes  play  a  primary  role  in  the  cause  of  ADHD. 
 Currently,  no  studies  have  identi�ed  a  speci�c  gene  that  causes  ADHD.  Part 
 of  the  di�culty  lies  in  the  complexity  of  the  phenotypes  and  relatively  small 
 e�ects  of  genetic  variants  13  .  This  section  will  lay  out  and  discuss  the 
 di�erent genes of interest that could possibly relate to the cause of ADHD. 

 Gene of Interest  Function in the Body  Relation to ADHD 

 Neurexin 1 
 (NRXN1) 

 Bind proteins → 
 Neurotransmitter release and 
 di�erentiation of synapse 

 Mutations in gene → 
 learning or memory 
 problems → ADHD 

 Dopamine 
 Receptor D3 
 (DRD3) 

 Controls cognition, impulse 
 control, attention, and sleep 

 Mutations in gene → 
 cognition and impulsiveness 
 problems → ADHD 

 Glutamic Acid 
 Decarboxylase 65 
 (GAD65) 

 Catalyzes the conversion of 
 glutamic acid into inhibitory 
 neurotransmitter γ-amino 
 butyric acid (GABA) → 
 neurotransmission 

 Serum of anti-GAD65 
 antibodies in patient → 
 ADHD 

 Patched Domain 
 Containing 1 gene 
 (Ptchd1) 

 Provides thalamic reticular 
 nucleus activity 

 Deletion of gene reduces 
 thalamic reticular nucleus 
 activity → attention de�cits 
 and hyperactivity → ADHD 

 Norepinephrine 
 Transporter 
 (SLC6A2) 

 Primary destruction mechanism 
 of noradrenaline (NE) and 
 involved in the reuptake of 
 dopamine (DA) and NE into the 
 presynaptic neuron 

 E�ects treatment of ADHD 
 (use of non-stimulants) v 

 Figure  1:  This  table  summarizes  the  �ve  genes  of  interest,  their  functions  in  
the  body, and its relation to ADHD. 

 5.1  Gene of Interest 1: Neurexin 1 (NRXN1) 

 The  �rst  gene  of  interest  is  a  family  of  cell  adhesion  proteins  called 
 neurexins.  Neurexins  are  encoded  mainly  by  NRXN1,  NRXN2,  and 
 NRXN3  genes  among  others  14  .  The  main  role  of  neurexins  in  the  cell 
 surface  of  the  neurons  is  to  bind  to  other  proteins  and  alpha-latrotoxin 
 presynaptic  receptors.  The  binding  of  these  proteins  can  in  return  lead  to 

 Berkeley Pharma Tech Journal of Medicine |  63 



 neurotransmitter  release  and  di�erentiation  of  synapse  15  .  However,  the 
 failure  to  bind  together  and  the  miscommunication  of  the  bindings 
 between  these  proteins  is  linked  to  a  speci�c  neurexin:  NRXN1  14  .  Along 
 with  playing  an  important  role  in  protein  binding,  another  crucial  role  of 
 NRXN1  is  helping  many  proteins  in  synaptic  transmission.  The  failure  of 
 NRXN1  to  carry  out  these  functions  within  the  cell  may  be  a  reason  for  the 
 development  of  learning  or  memory,  which  is  a  sign  of  ADHD  in  a 
 patient  15  . 

 There  are  some  in  vivo  studies  that  have  correlated  NRXN1  with  ADHD. 
 For  instance,  researchers  conducted  one  study  to  evaluate  the  protective 
 e�ect  and  potential  mechanism  of  NRXN1  on  learning  and  memory  in 
 ADHD  rats  15  .  The  methods  involved  grouping  the  four-week-old  rats  into 
 two  categories:  spontaneously  hypertensive  rats  (SHRs)  and  normal 
 Sprague  Dawley  (SD)  rats.  These  groups  of  rats  were  tested  by  using  a 
 Morris  water  maze  on  a  learning  and  memory  test.  Moreover,  qPCR  and 
 western  blots  were  used  to  analyze  the  expression  levels  of  NRXN1  at 
 mRNA  and  protein  levels.  It  was  concluded  that  the  overexpression  and 
 interference  of  NRXN1  played  a  role  in  impairing  the  ability  of  the  rats  to 
 learn  and  memorize  things  in  both  the  SHRs  and  SD  rats  15  .  However,  in  the 
 experiment,  a  portion  of  the  SD  rats  were  given  treatments  with 
 methylphenidate  (MPH)  during  the  trails.  This  was  shown  to  make  an 
 improvement  in  the  performance  of  the  treated  SD  rats.  The  change  in 
 NRXN1  in  the  rats  led  to  a  change  in  other  synapse-related  genes  including 
 PSD95,  SYN1,  GAP43,  and  NLGN1  genes.  Therefore,  it  can  be  concluded 
 that  NRXN1  de�ciency  is  associated  with  the  expression  of  synapse-related 
 genes  and  ADHD  pathogenesis  and  can  be  a  potential  therapeutic  target  for 
 ADHD treatment  15  . 

 5.2  Gene of Interest 2: Dopamine receptor 3 (DRD3) 

 Another  gene  of  interest  is  in  the  dopamine  receptor  family,  which  encodes 
 dopamine  receptors  D1,  D2,  D3,  D4,  and  D5  16  .  Dopamine  receptors  as  a 
 family  are  used  in  everyday  function.  It  a�ects  the  brain  as  it  is  able  to 
 control  and  process  emotions  and  movement  of  the  body  17  .  In  particular, 
 dopamine  receptor  D3  (DRD3)  a�ects  your  cognition,  impulse  control, 
 attention,  and  sleep  17  .  The  mutation  of  DRD3  mainly  leads  to  di�erent 

 Berkeley Pharma Tech Journal of Medicine |  64 



 diseases  such  as  Schizophrenia  and  Tremor.  These  mutations  can  be  caused 
 by  Ser-9-Gly,  a  nucleotide  polymorphism  in  DRD318.  Ser-9-Gly  has  a  C 
 allele in it which encodes glycine and a T allele which encodes serine  13  . 

 There  are  quite  a  few  in  vitro  studies  that  have  tried  to  correlate  DRD3 
 mutations  with  ADHD,  but  not  a  lot  of  them  have  been  successful  18  . 
 However,  there  is  a  DRD3  gene  and  ADHD  pharmco-behavioral  genetic 
 study  that  links  the  two  together  13  .  The  main  goal  of  the  study  was  to 
 examine  multiple  types  of  potential  genes  related  to  ADHD.  This  was  done 
 using  an  exploratory  analysis  with  a  comprehensive  approach.  575  children 
 with  ADHD  aged  6  to  12  were  the  subjects  of  the  study  and  were  assessed 
 under  three  of  the  experimental  conditions.  The  conditions  include  one 
 week  of  baseline  observation,  one  week  of  methylphenidate  (MPH),  and 
 one  week  of  placebo  18  .  Their  parents,  teachers,  and  research  sta�  evaluated 
 their  quantitative  behavioral  and  cognitive  dimensions  relevant  for  ADHD. 
 The  results  of  the  experiment  showed  a  nominal  association  between  the  T 
 allele  and  worse  behavioral  scores  while  the  subjects  were  in  the  MPH  week. 
 Along  with  that,  the  T  allele  demonstrated  a  nominal  association  with 
 increased  risk  for  ADHD,  response  to  placebo  and  MPH13.  The 
 conclusions  that  could  be  drawn  from  this  are  that  DRD3,  and  moreover 
 Ser-9-Gly,  play  a  role  in  the  cause  of  ADHD  and  variations  in  patient’s 
 behavior  18  . 

 5.3  Gene of Interest 3: Glutamic Acid Decarboxylase 65 (GAD65) 

 Glutamic  Acid  Decarboxylase  65  (GAD65)  is  another  gene  to  investigate  as 
 it  has  been  found  in  the  serum  of  patients  with  several  neurological 
 disorders.  GAD65  is  an  enzyme  that  is  produced  primarily  by  pancreatic 
 islet  cells  19  .  The  primary  role  of  GAD65  is  that  it  catalyzes  the  conversion  of 
 glutamic  acid  into  inhibitory  neurotransmitter  γ-amino  butyric  acid 
 (GABA)  that  is  present  in  synaptic  vesicles  of  GABAergic  neurons  for  its 
 release during inhibitory neurotransmission  20  . 

 Serum  anti-GAD65  antibodies  can  be  a  common  marker  of  subgroups  of 
 patients  with  autism  and  ADHD  as  shown  in  a  study  that  correlated  the 
 presence  of  GAD65  antibodies  in  the  serum  of  children  with  autism  or 
 ADHD  20  .  In  the  study,  there  were  14  normal  control  patients,  20  patients 
 with  autism,  and  15  patients  with  ADHD.  The  GAD65  antibodies  and 

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 total  IgG  were  assessed  in  the  serum  of  normal  patients  and  patients 
 diagnosed  with  either  autism  or  ADHD  20  .  In  conclusion,  none  of  the 
 normal  patients  had  GAD65  in  the  serum,  15%  of  children  with  autism  had 
 GAD65  detected,  and  27%  of  children  with  ADHD  had  GAD65  in  their 
 serum.  With  this,  60%  of  autistic  and  53%  of  ADHD  patients  reacted  with 
 Purkinje  neurons  in  mouse  cerebellum  and  20%  of  ADHD  patients'  serums 
 reacted  with  the  cells  in  the  molecular  and  granule  cell  layers  and  the  cells  in 
 the  vicinity  of  the  Purkinje  neurons  20  .  Therefore,  it  can  be  concluded  that 
 the  serum  anti-GAD65  antibodies  are  associated  with  patients  with  autism 
 and ADHD. 

 5.4  Gene  of  Interest  4:  Patched  Domain  Containing  1  gene 
 (Ptchd1) 

 The  Patched  Domain  Containing  1  gene  (Ptchd1)  is  another  gene  of 
 interest  as  many  studies  and  models  have  displayed  this  gene’s  role  in 
 ADHD.  Its  deletion  reduces  the  thalamic  reticular  nucleus  activity,  a  region 
 of  the  brain  that  synapses  the  entire  cortex  and  cerebellum.  Knockouts  of 
 this  gene  led  to  symptoms  of  attention  de�cits  and  hyperactivity  due  to  its 
 involvement  with  small  conductance  calcium-dependent  potassium 
 currents (SKs) within the thalamic reticular nucleus  21  . 

 In  one  of  these  experiments,  acute  injection  of  the  SK  positive  allosteric 
 modulator  1-ethyl-benzimidazolinone  EBIO  rescued  the  ADHD-like 
 knockout  behaviors  21  .  By  measuring  the  mouse’s  thalamic  activity  with  a 
 �uorescence  resonance  energy  transfer,  the  sensory-related  functions  of 
 mice  were  found  to  be  lower  in  knockouts  but  recovered  with  the  injection. 
 This  suggests  that  SK  channel  dysfunction  can  be  a  target  without  e�ects  on 
 aggression,  hypotonia,  and  learning  de�cits.  It  targets  only  inattention.  In 
 another  study,  Ptchd1  KO  mice  showed  drastic  changes  in  kynurenine 
 pathway  metabolite  concentrations  in  the  serum  and  the  brain,  indicating 
 that  the  activated  KP  is  associated  with  ADHD-like  behaviors.  This 
 pathway  is  implicated  in  generating  cellular  energy  in  the  form  of 
 nicotinamide  adenine  dinucleotide  (NAD+).  Because  energy  requirements 
 are  substantially  increased  during  an  immune  response,  the  KP  is  a  key 
 regulator  of  the  immune  system.  Having  the  Ptchd1  gene  have  a  close  tie  to 
 the  KP  pathway  indicates  the  association  between  ADHD  and  the 

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 anti-in�ammatory  responses  of  the  immune  system.  Global  PTCHD1 
 knockout  mice  were  used  to  measure  neuronal,  behavioral,  and  social 
 function  with  respect  to  a  gene  associated  with  ADHD  and  ASD-like 
 symptomatology.  Markers  of  symptomatology  can  be  determined  through 
 KP  impairments.  Thus,  there  is  potential  for  KP  to  be  used  as  a  clinical 
 biomarker when the PTCHD1 gene is inactivated  21  . 

 5.5  Gene of Interest 5: Norepinephrine Transporter (NET) 

 Atomoxetine  (ATX)  is  the  most  commonly  used  drug  in  a  non-stimulant 
 group  in  the  ADHD  treatment.  It  acts  by  increasing  the  levels  of  dopamine 
 (DA)  and  norepinephrine  (NE)  by  inhibition  of  presynaptic  NET  in  the 
 prefrontal  cortex  9  .  The  Norepinephrine  Transporter  (SLC6A2),  which  is 
 responsible  for  the  primary  destruction  mechanism  of  NE,  is  found  in  the 
 plasma  membrane  of  noradrenergic  neurons  involved  in  the  reuptake  of  DA 
 and  NE  into  the  presynaptic  neuron.  The  function  of  the  NE  transporter  is 
 attributed to multiple allelic variations of the SLC6A2 gene. 

 In  a  recent  study,  heterozygous  genotypes  rs12708954  genotypes  showed 
 greater  side  e�ects  during  treatment  than  normal  genotypes.  Similarly,  in 
 rs3785143  genotypes,  side  e�ects  in  heterozygous  carriers  have  been 
 reported  more  frequently  than  WT  carriers.  In  only  one  pilot  study, 
 rs3785143  T  allele  carriers  reported  a  loss  of  appetite  and  irritability  during 
 ATX  treatment  22  .  This  gene  polymorphism  implies  that  ADHD  genetic  risk 
 factors  not  only  in�uence  its  symptomatology,  but  also  modulate  the 
 e�ectiveness of stimulant treatment such as ATX on the patient’s response. 

 Future Investigations 

 ADHD  is  a  heritable  condition,  although  the  inheritance,  or  rather  the 
 likelihood  of  the  disease  being  passed  onto  the  next  generation,  is  complex. 
 While  ADHD  genetic  components  are  supported  by  twin  studies  and 
 slightly  less  so  by  GWAS  studies,  genetic  studies  provide  a  close  estimate  to 
 how  multiple  factors  could  intertwine  and  lead  to  comorbidities.  The 
 late-onset  form  of  ADHD  has  not  been  studied  enough.  Therefore, 

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 con�icting  results  on  genetic  studies  provide  little  information  about  the 
 late-onset of ADHD in adults compared to children. 

 Understanding  heritability,  long-term  causes,  and  environment-gene 
 interactions  are  required  in  whole-genome  sequencing  analyses.  As  of 
 current  literature,  genetic  studies  of  ADHD  have  been  targeted  to  risk 
 factors.  By  identifying  these  genetic  underpinnings,  it  could  reveal  whether 
 or  not  people  with  certain  genes  have  resilience  towards  ADHD  given  an 
 environmental  condition.  Understanding  this  interrelationship  between 
 genetic resilience and the genetic risk factors is important going forward. 

 Conclusion 

 Research  on  ADHD  and  ways  to  treat  it  have  been  researched  widely  in  the 
 past  several  years.  Current  treatments  mainly  include  the  use  of  stimulants 
 or  non-stimulants  as  medication.  Also,  cognitive  behavioral  therapy  (CBT) 
 is  another  popular  way  to  help  patients  deal  with  ADHD.  Along  with  this, 
 there  is  new  research  that  provides  evidence  that  ADHD  is  inheritable  and 
 can  run  in  families.  With  this  new  information,  it  can  lead  to  the  belief  that 
 focusing  on  gene  mutations  for  treatment  is  a  good  next  step  to  �nding  a 
 new  treatment  for  ADHD.  There  have  been  multiple  genes  that  have  been 
 discussed  including  Neurexins  1  (NRXN1),  Dopamine  receptor  D3 
 (DRD3),  Glutamic  Acid  Decarboxylase  65  (GAD65),  Patched  Domain 
 Containing  1  gene  (Ptchd1),  and  Norepinephrine  Transporter  (SLC6A2). 
 Multiple  in  vivo  studies  have  demonstrated  the  link  between  these  genes  and 
 ADHD.  While  all  of  this  is  known,  there  is  still  a  lot  to  learn  in  this  area. 
 There  is  a  lack  of  clinical  trials  and  testing  which  is  essential  to  determine 
 whether  or  not  these  genes  can  be  successfully  mutated  and  provide 
 signi�cant improvements to patients with ADHD. 

 Berkeley Pharma Tech Journal of Medicine |  68 



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