Contributions of Neuroscience Thesis

Contributions of Neuroscience to Our Understanding of Cognitive Development Adele Diamond1 and Dima Amso2

1 Department of Psychiatry, University of British Columbia, and Department of Child and Adolescent Psychiatry,

BC Children’s Hospital, Vancouver, Canada; and 2 Sackler Institute for Developmental Psychobiology,

Weill Medical College of Cornell University

ABSTRACT—One major contribution of neuroscience to

understanding cognitive development has been in demon-

strating that biology is not destiny—that is, demonstrating

the remarkable role of experience in shaping the mind,

brain, and body. Only rarely has neuroscience provided

wholly new insights into cognitive development, but often

it has provided evidence of mechanisms by which obser-

vations of developmental psychologists could be explained.

Behavioral findings have often remained controversial

until an underlying biological mechanism for them was

offered. Neuroscience has demonstrated promise for de-

tecting cognitive problems before they are behaviorally

observable—and, hence, promise for early intervention. In

this article, we discuss examples drawn from imitation and

mirror neurons, phenylketonuria (PKU) and prefrontal

dopamine, maternal touch and stress reactivity, and non-

genetic (behavioral) intergenerational transmission of bi-

ological characteristics.

KEYWORDS—plasticity; epigenesis; mothering; executive

functions; animal models; molecular genetics; memory

Neuroscience research has made its greatest contributions to the

study of cognitive development by illuminating mechanisms

(providing a ‘‘how’’) that underlie behavioral observations made

earlier by psychologists. It has also made important contribu-

tions to our understanding of cognitive development by dem-

onstrating that the brain is far more plastic at all ages than

previously thought—and thus that the speed and extent by which

experience and behavior can shape the brain is greater than al-

most anyone imagined. In other words, rather than showing that

biology is destiny, neuroscience research has been at the fore-

front of demonstrating the powerful role of experience throughout

life. Besides the surprising evidence of the remarkable extent

of experience-induced plasticity, rarely has neuroscience given

us previously unknown insights into cognitive development, but

neuroscience does offer promise of being able to detect some

problems before they are behaviorally observable.

PROVIDING MECHANISMS THAT CAN ACCOUNT FOR

BEHAVIORAL RESULTS REPORTED BY

PSYCHOLOGISTS

Here we describe two examples of behavioral findings by psy-

chologists that were largely ignored or extremely controversial

until underlying biological mechanisms capable of accounting

for them were provided by neuroscience research. One such

example concerns cognitive deficits documented in children

treated early and continuously for phenylketonuria (PKU). The

second example involves neonatal imitation observed by psy-

chologists and mirror neurons discovered by neuroscientists.

Prefrontal Dopamine System and PKU Cognitive Deficits

Since at least the mid-1980s, psychologists were reporting

cognitive deficits in children with PKU that resembled those

associated with frontal cortex dysfunction (e.g., Pennington,

VanDoornick, McCabe, & McCabe, 1985). Those reports did not

impact medical care, however. Doctors were skeptical. No one

could imagine a mechanism capable of producing what psy-

chologists claimed to be observing.

PKU is a disorder in the gene that codes for phenylalanine

hydroxylase, an enzyme essential for the conversion of phenyl-

alanine (Phe) to tyrosine (Tyr). In those with PKU, that enzyme is

Address correspondence to Adele Diamond, Canada Research Chair Professor of Developmental Cognitive Neuroscience, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, British Columbia, V6T 2A1, Canada; e-mail: adele. diamond@ubc.ca.

C U R R E N T D I R E C T I O N S I N P S Y C H O L O G I C A L S C I E N C E

136 Volume 17—Number 2Copyright r 2008 Association for Psychological Science

absent or inactive. Without treatment, Phe levels skyrocket,

resulting in gross brain damage and mental retardation. Phe is an

amino acid and a component of all dietary protein. PKU treat-

ment consists primarily of reducing dietary intake of protein to

keep Phe levels down, but that has to be balanced against the

need for protein. For years, children with PKU were considered

adequately treated if their blood Phe levels were below 600

micromoles per liter (mmol/L; normal levels in the general public being 60–120 mmol/L). Such children did not have mental re- tardation and showed no gross brain damage, although no one

disputed that their blood Phe levels were somewhat elevated and

their blood Tyr levels were somewhat reduced (Tyr levels were

not grossly reduced because even though the hydroxylation of

Phe into Tyr was largely inoperative, Tyr is also available in

protein). Since Phe and Tyr compete to cross into the brain, a

modest increase in the ratio of Phe to Tyr in the bloodstream

results in a modest decrease in how much Tyr can reach the

brain. Note that this is a global effect—the entire brain receives

somewhat too little Tyr. How was it possible to make sense of

psychologists’ claims that the resulting cognitive deficits were

not global but limited to the cognitive functions dependent on

prefrontal cortex?