A genotype of exceptional longevity
is associated with preservation of
N. Barzilai, MD; G. Atzmon, PhD; C.A. Derby, PhD; J.M. Bauman, MD; and R.B. Lipton, MD
Abstract—Objective: To test whether cholesterol ester transfer protein (CETP) genotype (VV homozygosity for I405V) is
associated with preservation of cognitive function in addition to its association with exceptional longevity. Methods: We
studied Ashkenazi Jews with exceptional longevity (n ? 158; age 99.2 ? 0.3 years) for the associations of CETP VV
genotype and lipoprotein phenotype, using the Mini-Mental State Examination (MMSE). To confirm the role of CETP in a
younger cohort, we studied subjects from the Einstein Aging Study (EAS) for associations between CETP VV and cognitive
impairment. Results: Subjects with MMSE ? 25 were twice as likely to have the CETP VV genotype (29% vs 14%,
p ? 0.02), and those with the VV genotype were more likely (61% vs 30%, p ? 0.02) to have MMSE ? 25. Subjects with the
VV genotype had lower levels of CETP (1.73 ? 0.11 vs 2.12 ? 0.10 ?g/mL, p ? 0.01), higher high-density lipoprotein
(HDL) levels (p ? 0.02), and larger lipoprotein particles (p ? 0.03). In the EAS cohort, an approximately fivefold
increase in the VV genotype (21% vs 4%, p ? 0.02), higher HDL levels, and larger lipoprotein particle sizes were
associated with less dementia and improved memory. Conclusions: Using two independent cohorts, we implicate the
longevity CETP gene as a modulator of age-related cognitive function. A specific CETP genotype is associated with
lower CETP levels and a favorable lipoprotein profile. It has not been determined whether modulation of this gene
prevents age-related decline or AD.
Exceptional longevity (i.e., living to 100) is rare, with
a prevalence of approximately 1 in 10,000 individu-
als in the general population.1Several mechanisms
have been proposed to explain this phenomenon. It
could reflect a delay or escape from age-related dis-
eases including cardiovascular disease (CVD), de-
mentia, and cancer. In addition, it may also reflect a
propensity to age slowly. Relatives of exceptionally
long-lived individuals are themselves much more
likely to be long lived, suggesting that heritable (ge-
netic) factors play a role.2,3
We recently showed that the relative frequency of
homozygosity (VV) for a common functional variant
(I405V) of the cholesterol ester transfer protein
(CETP) gene was enriched approximately threefold
to 25% in subjects with an average age of almost 100,
vs 8% in subjects roughly 30 years younger.4,5The
CETP VV genotype is associated with low plasma
levels of CETP, a protein involved in reverse choles-
terol transport. CETP mediates the exchange of cho-
lesteryl esters (CE) from high-density lipoprotein
(HDL) to apolipoprotein B (APOB)-containing li-
poproteins, promoting the subsequent uptake of cho-
lesterol by the liver.6Low CETP is also associated
with large low-density lipoprotein (LDL) and HDL
particle sizes, suggesting a direct functional effect of
Subjects with larger lipoproteins have a decreased
incidence of hypertension, CVD, and the metabolic
syndrome associated with aging.4
Recently, a study in the oldest old Italians living
around Florence7confirmed our results of a greater-
than-twofold enrichment of the favorable CETP (VV)
polymorphism. The VV genotype was associated with
lower CETP levels, larger LDL, and a lower preva-
lence of clinical endpoints. Although another study of
Italian centenarians8failed to show such an associa-
tion, this study included subjects from all of Italy,
where a strong genetic drift exists from north to
south, and the study did not look at other important
markers of lipoproteins and CETP levels. Other sup-
port for the importance of this pathway in excep-
tional longevity is rapidly accumulating. Japanese
centenarians have lower CETP levels and increased
lipoprotein particle sizes.9Furthermore, although
the Japanese do not have the same CETP polymor-
phism, subjects with a different polymorphism had
the lowest incidence of CHD.10
From the Institute for Aging Research (N.B., G.A., J.M.B., R.B.L.), Diabetes Research and Training Center (N.B., G.A., J.M.B.), Department of Neurology
(C.A.D., R.B.L.), and Department of Epidemiology and Population Health (C.A.D., R.B.L.), Albert Einstein College of Medicine, New York.
This work was supported by grants from the Einstein Aging Study PO-1 (AG-021654), the Paul Beeson Physician Faculty Scholar in Aging Award, the
Ellison Medical Foundation Senior Scholar Award, RO1 (AG-18728-01A1), the General Clinical Research Center (M01-RR12248), the Diabetes Research and
Training Center (DK 20541) at the Albert Einstein College of Medicine, and the Baltimore VA Geriatric Research and Education Clinical Center.
Disclosure: The authors report no conflicts of interest.
Received February 2, 2006. Accepted in final form September 12, 2006.
Address correspondence and reprint requests to Nir Barzilai, MD, Director: Institute for Aging Research, Belfer Bldg. #701, Albert Einstein College of
Medicine, 1300 Morris Park Avenue, Bronx, NY 10461; e-mail: email@example.com
Copyright © 2006 by AAN Enterprises, Inc.
In addition to protective effects against cardiovas-
cular disease, lipoproteins and their genotypes have
been linked to Alzheimer disease (AD). The APOE-?4
allele is the most common genetic risk factor for AD
identified to date. Some recent evidence suggests
that higher HDL cholesterol levels may protect
against cognitive decline associated with AD11and
other forms of dementia.12,13Furthermore, the
Laiden study demonstrated a significant association
between HDL and cognitive impairment in the oldest
patients.14Others have found that subjects with low
HDL levels (15%) had worse cognitive impairment,
but the same investigators could not show a relation-
ship between dyslipidemia and dementia or the role
of high HDL on cognitive function.15Centenarian
Ashkenazi Jews with the highest tertile of HDL lev-
els (average 75 mg/dL) had the best Mini-Mental
State Examination (MMSE) scores,16suggesting that
high HDL levels are protective. However, all of these
studies are different in the selection of the tested
population by age (90% were younger than 80 years
old), ethnicity, and technique of assessment. In addi-
tion, dementia is a risk factor for death, and pre-
longevity. Here, we test whether the effects of a fa-
vorable CETP genotype (405VV) and the associated
phenotype may be protective from decline in cogni-
tive function in centenarians, extending their effects
beyond the classic cardiovascular risks. To test this
hypothesis, we examined Ashkenazi Jewish subjects
with exceptional longevity to determine the relation
of cognitive function to CETP genotype and lipopro-
tein phenotype. In addition, we examined whether
this relationship would be present in a sample of
younger, community-dwelling elderly subjects.
(LonGenity). Ashkenazi Jews aged 95 to 107 years were recruited
as described elsewhere.3,4,16,17This is a unique population for ge-
netic studies because it is derived from an undetermined but
small number of founders (estimated to be several thousands) and
does not need to be stratified as is often necessary for other popu-
lations. One hundred fifty-eight subjects with exceptional longev-
ity (118 women and 40 men, age 99.2 (0.3) years [mean (SE); 48%
over the age of 100]) had a complete lipoprotein profile, genotypic
analysis, and a MMSE score. The participants’ ages were defined
by birth certificates or dates of birth as stated on passports. Sub-
jects were required to be living independently at 95 years of age as
a reflection of good health, although at the time of recruitment
they could be at any level of dependency.
A LonGenity research nurse visited the subjects in their homes
in the morning to draw a venous blood sample, obtain a medical
history, and perform a physical examination. Health histories
were obtained using a standardized questionnaire. All blood sam-
ples were processed at the General Clinical Research Center
(GCRC) at Albert Einstein College of Medicine.
A nurse practitioner administered the MMSE18to all partici-
pants in the morning hours. A score of more than 25 out of 30
points was considered indicative of good cognitive function,
whereas a score equal to or lower than 25 was considered indica-
tive of poor cognitive function.
Written informed consent was obtained in accordance with the
policy of the committee on clinical investigations of the Albert
Einstein College of Medicine.
Einstein Aging Study. The Einstein Aging Study (EAS) is a
community-based longitudinal study designed to identify predic-
tive factors for cognitive decline and dementia in a population-
Study design and subjects.
Longevity gene study
based study. The study design and recruitment methods have
been described previously.19,20Briefly, English-speaking subjects
older than 70 years of age were enrolled. Criteria for exclusion
included severe visual or hearing impairment and previous diag-
nosis of idiopathic PD, liver disease, alcoholism, or known termi-
nal illness. Subjects were screened to rule out the presence of
dementia at baseline.
At the inception of the study, the cohort was middle class, most
were Caucasian (91%), and the majority were women (64%).
Thirty-two percent were Ashkenazi Jews, who were used for this
study. Of the 173 subjects without baseline dementia who had
genotyping available, 124 subjects were between ages 75 and 85
and were followed longitudinally for an average of 4.6 years. Sub-
jects had fasting venous blood samples taken at the offices of the
EAS at Albert Einstein College of Medicine. All blood samples
were processed at the GCRC at Albert Einstein College of
Subjects received annual clinical assessments by a study neu-
rologist as well as a neuropsychological test battery.
The neuropsychological tests included the Blessed Information
Memory and Concentration (BIMC) test,21the digit-symbol subtest
of the Wechsler Adult Intelligence Scale,22a test of category fluen-
cy,23and free and cued selective reminding.24The presence of
dementia was determined by DSM-IV criteria, and subjects were
then case conferenced and subtyped by a neurologist.
Written informed consent was obtained at enrollment, and the
local institutional review board approved the study protocol.
Lipids and lipoproteins.
Total plasma cholesterol, triglycer-
ides, HDL, LDL, very-low-density lipoprotein (VLDL), and apoli-
poprotein A-I and B concentrations were performed by standard
automated methods at the clinical laboratories of Montefiore Med-
ical Center. LDL and HDL subclass levels and mean particle sizes
were determined by NMR spectroscopy at LipoScience, Inc. (Ra-
leigh, NC) as previously described.25,26Each NMR measurement
produces the concentrations of three LDL subclasses and five
HDL subclasses of varying size. From the LDL and HDL subclass
levels, weighted mean LDL and HDL particle sizes (diameter in
nanometers) were calculated.
Cholesteryl ester transfer protein genotyping and concentrations.
Lipoprotein sizes are largely determined by cholesteryl ester
transfer protein (CETP), in addition to other possible pathways,
thus providing the rationale to examine variations in these genes.
We genotyped several known CETP single-nucleotide polymor-
phisms (SNPs): in the promoter (-631) C/A (NCBI dbSNP
rs1800776) and (-629) C/A (rs1800775); I405V (rs5882) in exons 14
and D442G (rs2303790) in exons 15; and, in the first nucleotide in
intron 14, G/A. A multilocus (70 SNPs) PCR-based assay was used
to genotype these polymorphisms.27The CETP concentrations in
human serum were measured by ELISA (Wako Chemicals USA
Inc, Richmond, VA).
Pairwise crude comparisons of lipid lev-
els and lipid particle sizes among the study groups were carried
out using the Mann–Whitney U test because the distributions
were skewed. We conceptualized the study groups as forming an
ordered set, with subjects in the LonGenity study containing the
highest prevalence and the younger EAS subjects containing the
lowest prevalence of longevity-promoting genes and phenotypes.
Calculations were carried out using SAS version 6.12 (SAS
Institute, Cary, NC) and Stata version 8.0SE (Stata Corp., College
To account for false-positive associations resulting from multi-
ple tests of the 70 SNPs, a Bonferroni correction was applied to
determine the proper level of significance, p ? 0.05/70 ? 0.0007.
For a comparison of the difference in CETP I405V genotype
frequency between the groups, Hardy–Weinberg equilibrium was
tested, and a ?2test (Pearson) was performed. A p value less than
0.05 was considered the threshold for significance. Data are ex-
pressed as mean (SE).
with cognitive function.
five CETP polymorphic markers, only the common func-
tional I405V CETP variant (NCBI dbSNP rs5882) was sig-
nificantly associated with cognitive function. Subjects with
good cognitive function had a higher frequency of the
CETP VV genotype than those with poor cognitive function
CETP genotype and concentration associated
LonGenity.After analyzing the
December (2 of 2) 2006
(29% vs 14%, p ? 0.02) (figure, A. Conversely, those with
the CETP VV genotype were twice as likely (61% vs 30%,
p ? 0.02) to have good cognitive function than those with
the II genotype (not shown). Subjects with the VV geno-
type had significantly lower levels of CETP compared with
the II genotype (1.73 ? 0.11 vs 2.12 ? 0.10 ?g/mL). In
addition, CETP levels were significantly lower in those
with MMSE ? 25 (1.70 ? 0.07 ?g/mL) than in those with
MMSE ? 25 (1.90 ? 0.06 ?g/mL) (table 1).
After excluding centenarians with self-reported CVD
(n ? 101), those with good cognitive function still had a
significantly higher frequency of the favorable CETP geno-
type (VV) than those with poor cognitive function (31% vs
13%). When we excluded subjects with hypertension, those
with the VV genotype were twice as likely to have good
cognitive function compared with the non-VV genotype
(56% vs 28%, p ? 0.047), suggesting an independent effect
of the VV genotype on cognitive function. In the subjects
with reported hypertension, only 2 of the 36 subjects had
the VV genotype, and both of these had good cognitive
function. Those with a non-VV genotype were equally dis-
tributed among the good and poor cognitive function (52%
vs 47%, p ? 0.19).
Similar plasma albumin (3.89 ? 0.05 and 3.73 ? 0.04
g/dL) and urea nitrogen (25 ? 1 and 28 ? 2 mEq/L) levels
were seen in those with MMSE ? 25 and MMSE ? 25,
suggesting that nutritional status and poor hydration did
not influence MMSE testing in this population.
There were no gender differences according to MMSE
(42% of women and 45% of men centenarians had good
cognitive function, p ? 0.74) or genotypes (23% of women
and 25% of men centenarians had CETP VV, p ? 0.81).
Because the APOE genotype has been shown to be asso-
ciated with the risk for AD and CVD in the elderly,28we
also assessed its impact on cognitive function. Comparing
centenarian subjects with MMSE ? 25 vs those with
MMSE ? 25, similar frequencies of the APOE-?2 (4% vs
9%, p ? 0.1), APOE-?3 (88% vs 81%, p ? 0.2), and the
at-risk APOE-?4 allele (7% vs 10%, p ? 0.4) were noted.
After excluding those subjects with an APOE-ε4 allele, the
VV genotype was associated with a ?50% increase in good
cognitive function (64% vs 40%, p ? 0.042).
Our population was relatively educated, and we divided
the subjects into those with less than a high school educa-
tion vs those with at least some high school education.
There was no significant difference in the cognitive func-
tion between these two groups, suggesting that level of
education did not play a major role in our results.
EAS. One hundred seventy-three subjects without de-
mentia at baseline had genotyping available. The overall
prevalence of dementia in this group at the end of
follow-up was 17%. When we analyzed the longitudinal
cohort between ages 75 and 85 (n ? 124), 25 developed
dementia, representing 83% of all incident cases of demen-
tia. Subjects without dementia had an approximately five-
fold higher frequency of the CETP VV genotype than those
with dementia (21% vs 4%, p ? 0.02) (figure, B. There
were no gender differences according to cognitive function
(24% of women and 15% of men subjects had dementia,
Figure. (A) Proportion of centenarians with good (?25) vs
impaired (?25) cognitive function by Mini-Mental State
Examination (MMSE) as a function of CETP I405V geno-
type. * p ? 0.05. (B) Proportion of subjects in the EAS
with good vs impaired cognitive function as a function of
CETP I405V genotype. * p ? 0.05. II ? subjects homozy-
gous for isoleucine at position 405; VV ? subjects homozy-
gous for valine at position 405; IV ? subjects heterozygous
at position 405.
Table 1 Clinical and lipoprotein characteristics of subjects with
exceptional longevity according to cognitive function
MMSE ? 25
(n ? 90)
MMSE ? 25
(n ? 68)
Age, y 99.2 (0.3)99.1 (0.3)0.82
% women76 74 0.77
CETP, ?g/mL1.70 ? 0.071.90 ? 0.060.04
Cholesterol, mg/dL196 (4)207 (5)0.07
HDL, mg/dL51 (2)58 (2)0.02
Large HDL, % total58 (2)62 (2)0.04
HDL size, nm 9.42 (0.05) 9.59 (0.06)0.03
APOA1, mg/dL142 (3)155 (5)0.02
LDL, mg/dL113 (4)120 (4)0.16
Large LDL, % total 69 (3)73 (3)0.38
LDL size, nm21.4 (0.05)21.6 (0.06)0.03
APOB, mg/dL98 (3)94 (4)0.4
79 (4)70 (5) 0.13
22.2 (0.3) 23.1 (0.4)0.11
Cognitive function was determined by the 30-question Mini-
Mental State Exam (MMSE). Values are means (standard error).
CETP ? cholesterol ester transfer protein; HDL ? high-density
lipoprotein; APOA1 ? apolipoprotein A-I; LDL ? low-density li-
poprotein; APOB ? apolipoprotein B; VLDL ? very-low-density
lipoprotein; BMI ? body mass index.
December (2 of 2) 2006
p ? 0.26) or genotypes (17% of women and 19% of men
subjects had CETP VV, p ? 0.71).
When the frequencies of the APOE-?2, APOE-?3, and
APOE-?4 alleles were analyzed with respect to cognitive
function, similar frequencies were noted (5% vs 9% for
APOE-?2, 88% vs 79% for APOE-?3, and 7% vs 12% for
APOE-?4). In addition, after excluding those subjects with
an APOE-ε4 allele, none of the 15 subjects with dementia
had the VV genotype.
Association of lipoprotein levels and particle size with
good cognitive function had higher plasma HDL levels (p ?
0.02), larger average size of HDL particles (p ? 0.03), and
higher apolipoprotein A-I levels than those with impaired
cognitive function (p ? 0.02). MMSE demonstrated a sig-
nificant correlation with HDL particle size (r ? 0.2) and
plasma HDL levels (r ? 0.30). In addition, a higher propor-
tion of long-lived subjects had large HDL particle size (p ?
0.04). Although LDL particle size was slightly greater in
those with better cognitive function (p ? 0.03), LDL levels
and the percentage of large LDL lipoproteins had no rela-
tionship with MMSE score, nor did APOB or VLDL.
Even when subjects with CVD were excluded, HDL par-
ticle size remained significantly larger (9.62 ? 0.08 vs 9.41
? 0.06 nm, good vs poor cognitive function) among cente-
narians with good cognitive function, supporting an associ-
ation of lipoprotein particle size on cognitive function
independent of CVD.
EAS.Based on our finding of the relationship of HDL
particle size to cognitive function in the group of centenar-
ians, we independently examined the relationship of HDL
particle size to cognitive function and memory in an older
subgroup in the EAS study. Lipoprotein particle size was
analyzed in 35 subjects whose blood was drawn in parallel
to subjects in the LonGenity study. There was a significant
association of larger HDL particle size with better perfor-
mance in the BIMC test. A consistent trend for the other
tests was noted, such that those in the highest tertile of
HDL particle size tended to have better performance com-
pared with the lower tertiles (table 2). This effect was not
present for LDL particle size. Similar analyses examining
the relation of lipoprotein concentrations to cognitive per-
formance showed no consistent pattern to suggest that low
LDL was associated with better cognitive performance.
Long-lived subjects with
is increased monotonically in those surviving into
advance age, and it is overrepresented by nearly
The frequency of CETP VV genotype
threefold for 100 years of age compared with subjects
in their seventh decade of life.4This is the first re-
port to link this gene with specific protection against
age-related cognitive decline. This study links this
genotype with the phenotypic features including low
CETP level, higher HDL cholesterol level, and larger
lipoprotein particle size. It also confirms these re-
sults in a cohort that is approximately 20 years
A strength of this study is its use of a homogenous
population. Thus, although the genotype implicates
the gene involved, it is the level of expression and
effects on lipoprotein pattern that are clinically rele-
vant. Nevertheless, it was important to choose a sep-
arate Ashkenazi population
confirm the association of this genotype in addition
to the phenotype. Although the function of the CETP
I405V polymorphism has not been studied in vitro,
in population studies it has been associated with
lower plasma CETP levels, increased plasma HDL
levels, and increased lipoprotein particle size.4,29It is
known that CETP has a role in reverse cholesterol
transport, which is a cardioprotective function, and
lower levels would be thought to be harmful. How-
ever, lower levels of CETP are associated with in-
creased HDL levels and larger lipoprotein particle
size, and, in balance, the overall beneficial effect of
lower expression of CETP may be attributable to
these latter effects.30Alternatively, we recently
found that CETP is expressed in endothelial cells in
the brain (data not shown). This raises the possibil-
ity that just as APOE has a local effect in AD, CETP
may have a direct effect in the vasculature of the
brain, and lipoprotein characteristics in plasma may
simply be a marker for this protection.
CETP may help determine cognitive function of
the aging brain independent of the mechanisms for
the earlier onset of cognitive decline seen in AD,
which may be APOE dependent. We were interested
to see whether the APOE-?2 genotype might be pro-
tective for age-related decline in cognitive function.
APOE-?2 homozygosity was present in two of our
centenarians and in none from the younger cohort.
However, the frequency of the APOE-?2 allele in our
centenarian population (8.3%) was similar to the fre-
quency found in a population of Korean centenarians
Table 2 Median cognitive test scores by tertile of high-density lipoprotein size for 35 Ashkenazi Jews in the Einstein Aging Study who
were at least 85 years of age at time of blood draw
Tertile of high-density lipoprotein size
Memory and Concentration test
First: ? 8.9 nm, n ? 1123.025.022.0 6.0
Second: 8.9–9.27 nm, n ? 1125.0 32.029.0 4.0
Third: ? 9.27 nm, n ? 13 32.035.027.0 2.0
Kruskal–Wallace p value0.110.37 0.380.05
For the sum of free recall, category fluency, and digit-symbol tests, higher scores reflect better cognitive performance. For the Blessed
Information Memory and Concentration test, lower scores represent better function.
December (2 of 2) 2006
(6.3%).31The overall frequency of APOE-?2 in the
elderly Ashkenazi population was about 5%,32and
this frequency increased with aging.33Indeed, in the
younger control population in our previous study, the
APOE-?2 frequency was 4.4%, almost 50% lower
than in centenarians (p ? 0.007). Thus, the APOE-?2
genotype has no strong role in preservation of cogni-
tive function in this group of centenarians, although
its overrepresentation of its alleles in our centenari-
ans is interesting.
In support of a causal relationship between the
CETP genotype and phenotype, when we tested the
cognitive function of subjects with exceptional lon-
gevity, higher HDL levels and larger HDL particle
size were protective for cognitive decline. This sug-
gests that HDL may play a greater role than LDL in
protecting from cognitive decline associated with ag-
ing. Indeed, increased plasma levels of HDL (which
is correlated with HDL particle size in 70-year-old
subjects) may offer protection from AD11and other
forms of dementia.12,13Furthermore, in a group of
elderly subjects, reduced cognitive function was sig-
nificantly associated with low HDL levels, even after
subjects with CVD and stroke were excluded, sug-
gesting that HDL may be important in cognitive
function independent of CVD.14These findings sug-
gest pleiotropic effects of plasma HDL level and li-
poprotein particle size on both vascular disease and
To independently test our findings, we used data
from the EAS longitudinal prospective study. We
studied Ashkenazi Jews who were approximately 20
years younger and we assessed for any protective
influence of this favorable genotype and lipoprotein
phenotype on cognitive function. We confirmed that
the CETP VV genotype is protective and that plasma
HDL levels and larger HDL particle size may play a
protective role in maintaining the cognitive integrity
of the aging brain. The CETP VV genotype is much
less frequent in the younger subjects than in cente-
narians. Although in the younger cohort the overall
incidence of dementia was less than half compared
with those without this genotype, reaching trends in
all subjects and significance in the subjects aged 75
to 85 underlines the potential importance of this ge-
Because increased plasma levels of HDL may
offer protection from AD, a relevant question is
whether the CETP VV genotype and its lipoprotein
phenotype protects against age-related cognitive
decline as well as the development of AD. Two of
our centenarians were homozygous for APOE-?4;
one of them had good cognitive function compared
with one from our younger group of controls, sug-
gesting that other mechanisms may protect from
cognitive decline even in the presence of this
APOE-?4 genotype. It is also possible that the pro-
tective lipoprotein phenotype described here acts
downstream of other genetic and environmental
causes of dementia. Although the protective li-
poprotein phenotype could indicate favorable ef-
fects on the vascular integrity of the aging brain,
they could also have independent effects in brain
parenchyma. For example, HDL cholesterol in
vitro has antioxidative effects, which also could
mediate its protective effect on cognitive decline.34
The authors thank the participants and their families for their
participation. They also thank the following institutions that as-
sisted in recruitment: the Hebrew Home for the Aging, Riverdale,
NY; Kittay House, Bronx, NY; the Hebrew Home Hospital, West
Hartford, CT; and the Jewish Home for the Aged, New Haven, CT,
all under the aegis of the association for the Jewish Aging
Services, Washington, DC.
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NEW GUIDELINE PUBLISHED ON STATUS EPILEPTICUS IN CHILDREN
Don’t miss the AAN’s newest guideline, Diagnostic Assessment of the Child with Status Epilepticus, published in the
November 14, 2006, issue of Neurology. The guideline will help physicians determine the causes of SE, and reviews
evidence on the assessment of the child with SE. The guideline makes recommendations on the assessment of labora-
tory studies and metabolic and genetic testing, as well as obtaining EEGs and neuroimaging studies. SE occurs in over
30,000 children annually and is a life-threatening emergency that requires prompt recognition and immediate treat-
ment. For the full guideline and summaries to share with colleagues and patients, visit www.aan.com/Epilepticus.
December (2 of 2) 2006