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Cocaine Eats Up Brain Twice as Fast as Normal Aging
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Molecular Psychiatry (2013) 18, 134--135; doi:10.1038/mp.2012.31;
published online 24 April 2012
in all our research in HV around cognitive function & impairment with aging this subject gets no attention. Prior drug use, in this case cocaine, may be an important risk factor for premature cognitive decline in aging PWH. Jules Levin, NATAP
"the annual rate of global gray matter volume loss in cocaine-dependent individuals was almost twice the rate of healthy volunteers......Accelerated ageing in cocaine-dependent individuals was also demonstrated by a significant age-by-group interaction on gray matter volume of the regions affected by age.....As the psychological and physiological challenges of ageing may have also accelerated in individuals with long-term drug dependence,11 the effects of cocaine on the process of ageing should be recognized in order to design and administer age-appropriate treatments for older drug users."
"As we age, we all lose grey matter. However, what we have seen is that chronic cocaine users lose grey matter at a significantly faster rate, which could be a sign of premature ageing."
Dr Karen Ersche, of the Behavioural and Clinical Neuroscience Institute (BCNI) at the University of Cambridge
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Cocaine may speed up the aging of the brain, according to new research that finds that people who are addicted to the drug lose twice the brain volume each year as non-drug users.
Cocaine-dependent individuals anecdotally appear aged and their mortality rates are estimated up to eight times higher than in the healthy population.1 Psychological and physiological changes typically associated with old age such as cognitive decline, brain atrophy, or immunodeficiency are also seen in middle-aged cocaine-dependent individuals.2,3 These observations raise the question of whether cocaine abuse might accelerate the process of normal ageing. Although this is a little-studied area, there are several reasons for assuming that chronic cocaine exposure interferes with the processes of brain ageing.
We compared the effects of age on gray matter volume in 120 individuals aged 18--50 years (Supplementary Information). Half of the sample met the standard diagnostic criteria for cocaine dependence of the DSM-IV-TR;4 whereas the other half had no history of substance misuse disorders or major psychiatric disorders. The two groups were matched for age (t118.0.12, P.0.905), gender (w2.2.8, P.0.148), and verbal IQ (t115.0.36, P.0.716), as described elsewhere.5 All participants underwent a structural MRI brain scan, which was analyzed using voxel-based morphometry5 to produce whole-brain maps of age-related change in gray matter volume.
All participants showed a reduction of gray matter volume in cortical and subcortical regions as a linear function of increasing
calendar age (Figures 1a and b). However, the annual rate of global gray matter volume loss in cocaine-dependent individuals was almost twice the rate of healthy volunteers (that is, 3.08 ml per year (standard error (s.e.): 0.49 ml) versus 1.69 ml per year (s.e.: 0.41 ml)). Consequently, the rate of age-related gray matter volume loss in cocaine-dependent individuals was significantly greater than in healthy volunteers (F1,116.4.7, P.0.031); this interaction remained significant after excluding 16 individuals with comorbid alcohol dependence (F1,100.6.4, P.0.013).
Accelerated ageing in cocaine-dependent individuals was also demonstrated by a significant age-by-group interaction on gray matter volume of the regions affected by age (Po0.001, see Figure 1c). Cocaine-dependent individuals showed a significantly greater-than-normal age-related decline in gray matter in prefrontal and temporal regions compared with healthy controls.
By contrast, parts of the striatum appeared resistant to age-related volume decline in the cocaine-using group. Enlarged striatal volume has frequently been reported in stimulant-dependent individuals,5,6 possibly reflecting a marker of reduced dopamine neurotransmission in this dopamine-rich brain region where drugs like cocaine work. Decline in striatal dopamine receptor density has been associated with normal age-related cognitive decline.7
The relative absence of age-related changes in the striatum of cocaine-dependent people may thus reflect another feature of an
abnormal brain ageing process.
Abnormal ageing in chronic cocaine users is an emerging public health concern, which has received little attention. Approximately
1% (ref. 8) of the 21 million users of cocaine wordwide,9 are considered to develop cocaine dependence. These individuals may potentially be at risk of premature brain ageing.
Young people taking cocaine today need to be educated about the longterm risk of ageing prematurely, specifically at a time when many developed economies are facing the demographic challenge of an ageing population. Our findings also draw attention to the increasing number of older drug users seeking treatment for drug abuse.10 Drug-treatment services, however, mainly target drug use in young people, focusing on prevention and harm reduction; the needs of older drug users are not so well catered for. As the psychological and physiological challenges of ageing may have also accelerated in individuals with long-term drug dependence,11 the effects of cocaine on the process of ageing should be recognized in order to design and administer age-appropriate treatments for older drug users.
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