Release Date:  March 9, 2000
RFA:  NS-01-004

National Institute of Neurological Disorders and Stroke


Letter of Intent Receipt Date:  June 1, 2000
Application Receipt Date:       July 26, 2000


The purpose of this RFA is to solicit research on the etiology and treatment 
of spinal muscular atrophy, amyotrophic lateral sclerosis, and other motor 
neuron diseases.  Considerable progress has been made in recent years toward 
understanding the biological bases of these diseases.  In particular, 
important steps have been taken in identifying the genetic defects underlying 
certain motor neuron diseases, and in the development of animal models for 
these diseases.  However, much remains to be learned about the mechanisms 
through which genetic mutations and other biological insults lead to 
pathology, and how these mechanisms may be manipulated therapeutically.  This 
RFA will solicit novel approaches to understanding and treating motor neuron 
diseases, with emphasis on cellular, molecular, and high throughput 


Motor neuron diseases are among the most devastating of neurological 
disorders.  These fatal diseases progressively paralyze the body, while 
leaving the mind intact and aware. The most common motor neuron diseases are 
spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS).  Both 
of these diseases are comparatively frequent, with an annual incidence of 3 
per 100,000 reported for ALS and a frequency of one in 10,000 live births 
observed for SMA. No cure, and little in the way of effective treatment, 
currently exists for these diseases.  However, major advances have been made 
recently in our understanding of the genetic bases of these diseases, as well 
as in the molecular and developmental biology of motor neurons.  Thus, now is 
an opportune time to launch a strong attack on these diseases.

Both SMA and ALS have as their cardinal feature the loss of spinal motor 
neurons.  In other respects, however, the two diseases are quite different.  
SMA generally has a very early onset (generally between 0 and 18 years), 
whereas ALS usually does not strike until middle age or later.  SMA is an 
inherited disease and results from mutations in a single gene, the survival 
of motor neuron 1 (SMN1) gene.  ALS has both familial and sporadic forms, and 
the familial forms have now been linked to several distinct genetic loci.  
ALS has prominent upper as well as lower motor neuron involvement, whereas 
SMA is confined to lower motor neurons.

In addition to SMA and ALS, there are several other diseases that involve 
degeneration of lower and/or upper motor neurons.  Of these, spinobulbar 
muscular atrophy (SBMA) is the most common.  As the name implies, there are 
prominent bulbar signs and loss of brainstem motor neurons in this disorder.  
SBMA can have its onset in either childhood or adulthood. It is an X-linked 
recessive disorder resulting from an expansion of the CAG repeat in the 
androgen receptor gene.  

Despite differences in etiology, SMA, ALS, and other motor neuron disorders 
have commonalities in terms of potential treatment strategies.  First, the 
fact that motor neurons are a relatively discrete, homogeneous, and well-
characterized cell population makes these diseases particularly amenable to 
gene stem cell replacement therapy and/or gene therapy.  Second, while the 
upstream events that trigger the onset of these diseases may differ, the fact 
that they specifically affect motor neurons raises the possibility of common 
downstream targets for drug intervention.  

The National Institute of Neurological Disorders and Stroke invites 
applications for research on the molecular and cellular mechanisms of SMA, 
ALS, and other motor neuron disorders, and on the development of potential 
therapeutics for these diseases.  Studies using novel approaches or 
technologies or addressing novel hypotheses are particularly encouraged.  
Specific areas of interest include, but are not limited to, the topics listed 
Objectives and Scope

Research Priorities for SMA

Major strides were made recently in SMA research with the identification of 
the SMN gene and the development of the first animal models for SMA.  Rapid 
progress has also been made in understanding the function of the SMN protein.  
Despite these important advances, however, our understanding of SMA remains 
fragmentary.  In particular, very little is known about the natural history 
or cellular mechanisms of motor neuron loss in SMA.  Central questions 
include the following:  what is the time course of motor neuron loss relative 
to neuronal differentiation, axon outgrowth, target contact, and the 
development of presynaptic inputs?  Do motor neurons differentiate in normal 
numbers and then die off, or is there also a failure of motor neuron 
differentiation?  What proportion of motor neurons are lost by the time a 
patient or animal model shows signs of muscle weakness?  Is ongoing motor 
neuron loss a significant component of the natural history of SMA?  The 
answers to these questions are crucial for the rational design of 
therapeutics, and also to establish the developmental window during which 
such therapeutics are likely to be most efficacious.

A second major area of inquiry concerns the molecular mechanisms through 
which mutations in the SMN gene lead to cellular pathology.  There is now 
strong evidence that SMN normally functions to modulate RNA splicing, 
possibly via regulation of spliceosomal small nuclear ribonucleoprotein 
particle (snRNP) biogenesis.  However, the precise mechanisms through which 
loss of SMN protein causes motor neuron death are unclear.  In particular, 
there is a need to obtain more precise data about the spatial and temporal 
pattern of SMN1 expression in human and animal models, and to compare the 
normal time course of SMN expression with the time course of motor neuron 
development.  Second, it will be important to determine when the first signs 
of motor neuron deterioration occur in SMN-deficient models relative to the 
normal time of onset of SMN1 expression.  Finally, microarray-based profiling 
of gene expression in normal and SMN-deficient motor neurons should offer 
insights into the time course and molecular basis of motor neuron death.

These and other research priorities for SMA are summarized below:

O Determine the time course and cellular mechanisms of motor neuron loss in 
vivo, both in humans and in animal models

O Develop additional animal models of SMA

O Identify the RNA substrates on which SMN-regulated spliceosomes normally 
act (particularly those substrates specific to motor neurons)

O Look for motor neuron-specific binding partners of SMN

O Determine if SMN protein is involved in cellular functions other than RNA 

O Understand the mechanisms regulating expression and function of the SMN1 
and SMN2 genes

O Elucidate the downstream molecular changes caused by loss of SMN function

Research Priorities for ALS

ALS has a more complex genetic basis than SMA, with only 5-10% of ALS cases 
being familial.  Of these, 15-20% are due to mutations in the gene encoding 
Cu/Zn superoxide dismutase 1 (SOD).  These appear to be gain-of-function 
mutations that confer toxic properties on the enzyme.  The discovery of SOD 
mutations as a cause for ALS has allowed some progress to be made in 
understanding the disease:  animal models for the disease are now available, 
and hypotheses are being developed and tested concerning the molecular events 
leading to cell death.  Nevertheless, SOD mutations are responsible for a 
relatively small proportion of cases of familial ALS.  A fuller understanding 
of ALS may therefore come from the study of other etiologies.

Perhaps an even more pressing need, in terms of the number of patients 
affected, is to learn more about the causes of sporadic ALS.  Recent work has 
demonstrated defective splicing of RNA for a glutamate transporter in a very 
high proportion (60-70%) of sporadic cases of ALS.  Additional common 
molecular defects in sporadic ALS might be discovered through the use of 
genome scanning methods or high throughput analyses of gene and protein 
expression. Given the possible role of oxidative stress in the etiology of 
ALS, mitochondrial genes and proteins could be an important focus for such 

These and other research priorities for ALS are summarized below:

O Identify additional genetic loci associated with familial ALS

O Look for acquired gene mutations in sporadic ALS

O Perform global analyses of gene and protein expression in human and animal 
models of ALS

O Identify new (non-SOD) animal models for ALS (for example, through 
collaborations with large-scale mouse mutagenesis centers)

O Understand the mechanism of upper motor neuron cell death in ALS

O Analyze cellular and molecular pathology of glial cells in human and 
animal models of ALS

O Explore potential non-cell autonomous mechanisms of ALS

O Proposals for research on normal and abnormal SOD function are not 
encouraged because this topic is already receiving relatively intensive 

Research Priorities Relevant to All Motor Neuron Diseases

Although SMA, ALS, and SBMA have differences in etiology and clinical time 
course, all three diseases are characterized by the loss of spinal motor 
neurons.  The reasons for the selective vulnerability of motor neurons in 
these diseases are not understood.  This vulnerability does not appear to 
result from selective expression of mutant gene products: the SMN, SOD, and 
androgen receptor genes all are expressed in a variety of both neuronal and 
nonneuronal cell types in addition to motor neurons.  However, it is possible 
that the development or maintenance of motor neurons requires unique proteins 
(or combinations thereof) that either by themselves or by the selective 
requirement for them render motor neurons especially vulnerable to changes in 
SMN, SOD, or androgen receptor gene function.  Alternatively, the unusually 
high metabolic rates and/or long axonal projections of motor neurons may 
render them vulnerable via elevated requirements for common neuronal 
housekeeping proteins.  In this regard, it is notable that different subsets 
of motor neurons are differentially affected in these disorders.  Finally, it 
is of interest to note that defects in RNA splicing mechanisms have been 
implicated in both SMA and ALS.  Thus, further study of RNA splicing 
mechanisms in motor neurons is clearly warranted.  In particular, are there 
spliceosomal proteins or RNAs found only in motor neurons? Are there motor 
neuron-specific substrates for RNA splicing?  Does the profile of motor 
neuron spliceosomal components or substrates change with age? 

SMA, ALS, and SBMA also have commonalities in terms of treatment strategy.  
Because these diseases involve loss of lower motor neurons, a relatively 
discrete and well-characterized cell population, they may be especially good 
targets for stem cell therapy.  Purified motor neuron cell lines have been 
developed in vitro, and embryonic stem cells (ES cells) also show promise for 
replacing motor neurons.  Further characterization and testing of these cells 
in vitro and in mouse models of motor neuron diseases are a high priority.  

An additional area of high priority is the development of high throughput 
methods for screening potential therapeutic agents.  New methods in 
combinatorial chemistry have been used to generate large libraries of 
molecules;  collections of natural products also exist.  Screening of such 
collections may lead to the identification of therapeutic agents for motor 
neurons disorders.  What is needed to unleash the potential of these 
libraries are high throughput assays with which to screen molecules for 
therapeutic activity.  These assays could be either cell-free or whole-cell 
in vitro assays of the expression, activity, or aggregation of proteins 
implicated in motor neuron disease pathogenesis.  Also of high priority is 
the development of efficient methods for secondary testing of therapeutic 
agents in animal models of motor neuron disease.  These methods do not 
necessarily have to be limited to mouse models, but could include lower 
vertebrates and invertebrates (such as Drosophila) as well.

O Understand why motor neurons are selectively vulnerable to the toxic 
effects of certain gene mutations

O Characterize mechanisms and substrates of RNA splicing in motor neurons 
and define changes in these over the lifespan

O Develop new motor neuron cell lines for transplantation or testing of 
therapeutic agents

O Refine and test currently available stem cell lines for therapeutic 
efficacy in animal models, with emphasis on eventual application in humans

O Develop high efficiency methods for gene delivery to motor neurons

O Develop high throughput in vitro assays for screening potential 
therapeutic agents

O Develop efficient assays for motor neuron function in animal models (for 
use in testing therapeutic agents or in identifying mutations affecting 
motor neurons in large-scale mutagenesis projects)

O Identify early surrogate markers for motor neuron disease


During the course of the award period, the Principal Investigators may be 
invited to meet with NIH program staff in Bethesda, MD, to review scientific 
progress. Other scientists external to and knowledgeable about this area of 
research may also be invited to participate. Budget requests should assume 
that the travel funds will be needed for the PI to meet annually in the 
Washington, D.C. area, should such meetings be advisable.

Progress toward understanding and treating motor neuron diseases will be 
facilitated by the timely and broad dissemination of research resources 
(including sequence data, animal models, cell lines, and technological 
advances) acquired by research funded by this RFA. Thus, applications 
submitted in response to this RFA must include a discussion of plans for 
making available data and materials acquired during the proposed project.


This RFA will use the National Institutes of Health (NIH) research project 
grant (R01) and Exploratory/Development Research Grant (R21) award 
mechanisms. Responsibility for the planning, direction, and execution of the 
proposed project will be solely that of the applicant.

The total project period for an application for an R01 award submitted in 
response to this RFA may not exceed 5 years.

The R21 awards are to demonstrate feasibility and to obtain preliminary data 
testing innovative ideas that represent a clear departure from ongoing 
research interests. These grants are intended to 1) provide initial support 
for new investigators; 2) allow exploration of possible innovative new 
directions for established investigators; and 3) stimulate investigators from 
other areas to lend their expertise to research within the scope of this 
solicitation. Applicants for the R21 must limit their requests to $100,000 
direct costs per year and are limited to two years. These R21 grants will not 
be renewable;  continuation of projects developed under this program will be 
through the regular research grant (R01) program.

This RFA is a one-time solicitation. Future unsolicited competing 
continuation applications will compete with all investigator-initiated 
applications and be reviewed according to the customary peer review 
procedures.  The anticipated award date is April 1, 2001.


NINDS intends to commit approximately $3 million in FY 2001 to fund 8 to12 
new grants in response to this RFA. An applicant may request a project period 
of up to 5 years for an R01 award and 2 years for an R21 award.  Because the 
nature and scope of the research proposed may vary, it is anticipated that 
the size of each award will also vary. Although the financial plans of NINDS 
provide support for this program, awards pursuant to this RFA are contingent 
upon the availability of funds and the receipt of a sufficient number of 
applications of outstanding scientific and technical merit. 


Applications may be submitted by domestic and foreign, for-profit and non-
profit organizations, public and private, such as universities, colleges, 
hospitals, laboratories, units of State and local governments, and eligible 
agencies of the Federal government. Racial/ethnic minority individuals, 
women, and persons with disabilities are encouraged to apply as Principal 


Inquiries concerning this RFA are encouraged. The opportunity to clarify any 
issues or questions from potential applicants is welcome.

Direct inquiries regarding programmatic issues to:

Gabrielle G. Leblanc, Ph.D.
Program Director, Neurodevelopment
National Institute of Neurological Disorders and Stroke
Neuroscience Center, Suite 2136, MSC 9523
6001 Executive Boulevard
Bethesda, MD 20892-9523  (Rockville, MD 20852 for express, courier service)
Phone:  301-496-5745
FAX:  301-402-1501
E-mail:  GL54h@nih.gov

Direct inquiries regarding fiscal matters to:

Tina M. Carlisle
Grants Management Specialist
National Institute of Neurological Disorders and Stroke
6001 Executive Boulevard, Suite 3264, MSC 9537
Bethesda, Maryland  20892-9537
Phone:  (301) 496-3938  
FAX:  (301) 402-0219
Email: carlislt@ninds.nih.gov


Prospective applicants are asked to submit a letter of intent that includes a 
descriptive title of the proposed research, the name, address, and telephone 
number of the Principal Investigator, the identities of other key personnel 
and participating institutions, and the number and title of the RFA in 
response to which the application may be submitted.  Although a letter of 
intent is not required, is not binding, and does not enter into the review of 
a subsequent application, the information that it contains allows NINDS staff 
to estimate the potential review workload and plan the review.

The Letter of Intent is to be sent to:

Gabrielle G. Leblanc, Ph.D.
Program Director
Neurodevelopment Program
National Institute of Neurological Disorders and Stroke
Neuroscience Center, Suite 2136, MSC 9523
6001 Executive Boulevard
Bethesda, MD 20892-9523  (Rockville, MD 20852 for courier service)
Phone:  301-496-5745
FAX:  301-402-1501
E-mail:  GL54h@nih.gov


Letter of Intent Receipt Date:  June 1, 2000
Application Receipt Date:  July 26, 2000
Peer Review Date:  November 2000
Council Review:  February 2001
Earliest Start Date:  April 1, 2001


The research grant application form PHS 398 (rev. 4/98) is to be used in 
applying for these grants. These forms are available at most institutional 
offices of sponsored research and from the Division of Extramural Outreach 
and Information Resources, National Institutes of Health, 6701 Rockledge 
Drive, MSC 7910, Bethesda, MD 20892-7910, telephone 301/710-0267, email: 

The RFA title and number must be typed on line 2 of the face page of the 
application form and the “YES” box must be marked.  In addition, the RFA 
label available in the PHS 398 (rev. 4/98) application form must be affixed 
to the bottom of the face page of the application. Failure to use this label 
could result in delayed processing of the application such that it may not 
reach the review committee in time for review. 

The sample RFA label available at: 
https://grants.nih.gov/grants/funding/phs398/label-bk.pdf has been modified 
to allow for this change. Please note this in in pdf 


PHS 398

The modular grant concept establishes specific modules in which direct costs 
may be requested as well as a maximum level for requested budgets. Only 
limited budgetary information is required under this approach.  The just-in-
time concept allows applicants to submit certain information only when there 
is a possibility for an award. It is anticipated that these
changes will reduce the administrative burden for the applicants, reviewers 
and Institute staff. Applications that request more than $250,000 direct 
costs in any year must follow the traditional PHS 398 application 
instructions. The total direct costs must be requested in accordance with the 
program guidelines and the modifications made to the standard PHS 398 
application instructions described below. 

o FACE PAGE: Items 7a and 7b should be completed, indicating Direct Costs (in 
$25,000 increments up to a maximum of $250,000) and Total Costs [Modular 
Direct plus Facilities and Administrative (F&A) costs] for the initial budget
period. Items 8a and 8b should be completed indicating the Direct and Total
Costs for the entire proposed period of support. 

of the PHS 398. It is not required and will not be accepted with the

categorical budget table on Form Page 5 of the PHS 398. It is not required 
and will not be accepted with the application. 

o NARRATIVE BUDGET JUSTIFICATION: Use a Modular Grant Budget Narrative page 
(https://grants.nih.gov/grants/funding/modular/modular.htm for sample pages). 
At the top of the page, enter the total direct costs requested for each year. 

o Under Personnel, list key project personnel, including their names, percent 
of effort, and roles on the project. No individual salary information should 
be provided. However, the applicant should use the current NIH salary cap 
level and the NIH policy for graduate student compensation in developing the 
budget request.

o Consortium/Contractual costs, provide an estimate of total costs (direct
plus facilities and administrative) for each year, each rounded to the 
$1,000. List the individuals/organizations with whom consortium or
contractual arrangements have been made, the percent effort of key personnel,
and the role on the project. Indicate whether the collaborating institution
is foreign or domestic. The total cost for a consortium/contractual
arrangement is included in the overall requested modular direct cost amount. 

o Provide an additional narrative budget justification for any variation in
the number of modules requested beyond the first year.

o BIOGRAPHICAL SKETCH: The Biographical Sketch provides information used by 
reviewers in the assessment of each individual's qualifications for a 
role in the proposed project, as well as to evaluate the overall
qualifications of the research team. A biographical sketch is required for
all key personnel, following the instructions below No more than three pages
may be used for each person. A sample biographical sketch may be viewed at:

-Complete the educational block at the top of the form page
-List position(s) and any honors
-Provide information, including overall goals and responsibilities, on
research projects ongoing or completed during the last three years
-List selected peer-reviewed publications, with full citations

o CHECKLIST - This page should be completed and submitted with the 
application. If the F&A rate agreement has been established, indicate the 
type of agreement and the date. All appropriate exclusions must be applied in 
the calculation of the F&A costs for the initial budget period and all future 
budget years.

o The applicant should provide the name and phone number of the individual to 
contact concerning fiscal and administrative issues if additional information 
is necessary following the initial review.

Submit a signed, typewritten original of the application, including the 
Checklist, and three signed photocopies, in one package to:

BETHESDA, MD 20892-7710
BETHESDA, MD 20817 (for express/courier service)

At the time of submission, two additional copies of the application must be 
sent to:

Dr. Lillian Pubols
Scientific Review Branch
National Institute of Neurological Disorders and Stroke
6001 Executive Blvd., Suite 3208, MSC 9529
Bethesda, MD 20892-9529 (Rockville, MD 20852 for express/courier service)
Telephone: (301) 496-9223
FAX: (301) 402-0182
Email: LP28E@nih.gov

Applications must be received by the application receipt date listed in the 
heading of this RFA. If an application is received after that date, it will 
be returned to the applicant without review.
The Center for Scientific Review (CSR) will not accept any application in 
response to this RFA that is essentially the same as one currently pending 
initial review, unless the applicant withdraws the pending application. The 
CSR will not accept any application that is essentially the same as one 
already reviewed. This does not preclude the submission of substantial 
revisions of applications already reviewed, but such applications must 
include an introduction addressing the previous critique.


Upon receipt, applications will be reviewed for completeness by the CSR and 
responsiveness by NINDS.  If the application is not responsive to the RFA, 
NINDS staff may contact the applicant to determine whether to return the 
application to the applicant or submit it for review in competition with 
unsolicited applications at the next review cycle.

Applications that are complete and responsive to the RFA will be evaluated 
for scientific and technical merit by an appropriate peer review group 
convened by NINDS in accordance with the review criteria stated below. As 
part of the initial merit review, all applications will receive a written 
critique and undergo a process in which only those applications deemed to 
have the highest scientific merit, generally the top half of the applications 
under review, will be discussed, assigned a priority score, and receive a 
second level review by the NINDS National Advisory Council.

Review Criteria

The goals of NIH-supported research are to advance our understanding of 
biological systems, improve the control of disease, and enhance health. In 
the written comments reviewers will be asked to discuss the following aspects 
of the application in order to judge the likelihood that the proposed 
research will have a substantial impact on the pursuit of these goals. Each 
of these criteria will be addressed and considered in assigning the overall 
score, weighting them as appropriate for each application. Note that the 
application does not need to be strong in all categories to be judged likely 
to have major scientific impact and thus deserve a high priority score. For 
example, an investigator may propose to carry out important work that by its 
nature is not innovative but is essential to move a field forward.

(1) Significance: Does this study address an important problem or develop 
an important technology? If the aims of the application are achieved, how 
will scientific knowledge or technological capability be advanced? What 
will be the effect of these studies on the concepts or methods that drive 
this field?

(2) Approach: Are the conceptual framework, design, methods, and analyses 
adequately developed, well-integrated, and appropriate to the aims of the 
project? Does the applicant acknowledge potential problem areas and 
consider alternative tactics?

(3) Innovation: Does the project employ novel concepts, approaches or 
method? Are the aims original and innovative? Does the project challenge 
existing paradigms or develop new methodologies or technologies?

(4) Investigator: Is the investigator appropriately trained and well suited 
to carry out this work? Is the work proposed appropriate to the experience 
level of the principal investigator and other researchers (if any)?

(5) Environment: Does the scientific environment in which the work will be 
done contribute to the probability of success? Do the proposed experiments 
take advantage of unique features of the scientific environment or employ 
useful collaborative arrangements? Is there evidence of institutional 

In addition to the above criteria, in accordance with NIH policy, all 
applications will also be reviewed with respect to the following:

o Adequacy of plans for dissemination of research resources:  What is the 
likelihood that any research resources (including sequence data, animal 
models, cell lines, and technological advances) generated by the project will 
be made widely available in a timely fashion to the scientific community?  
Applicants should include in their applications a discussion of their plans 
for making available research resources acquired during the proposed project. 
The initial review group will be asked to comment the adequacy of these plans 
for making available research resources.  Any opinions expressed by reviewers 
about this aspect of the proposal will be recorded as an administrative note.
o The adequacy of plans to include both genders, minorities and their 
subgroups, and children as appropriate for the scientific goals of the 
research. Plans for the recruitment and retention of subjects will also be 
o The reasonableness of the proposed budget and duration in relation to the 
proposed research
o The adequacy of the proposed protection for humans, animals or the 
environment, to the extent they may be adversely affected by the project 
proposed in the application.


Award criteria that will be used to make award decisions include:
o scientific merit (as determined by peer review);
o adequacy of plans to make widely available to the research community all 
research resources developed during this project;
o availability of funds;
o programmatic priorities.


It is the policy of the NIH that women and members of minority groups and 
their subpopulations must be included in all NIH supported biomedical and 
behavioral research projects involving human subjects, unless a clear and 
compelling rationale and justification is provided that inclusion is 
inappropriate with respect to the health of the subjects or the purpose of 
the research. This policy results from the NIH Revitalization Act of 1993 
(Section 492B of Public Law 103-43).

All investigators proposing research involving human subjects should read the 
"NIH Guidelines for Inclusion of Women and Minorities as Subjects in Clinical 
Research," which was published in the Federal Register of March 28, 1994 (FR 
59 14508-14513) and in the NIH Guide for Grants and Contracts, Vol. 23, No. 
11, March 18, 1994, available on the web at: 


It is the policy of NIH that children (i.e., individuals under the age of 21) 
must be included in all human subjects research, conducted or supported by 
the NIH, unless there are scientific and ethical reasons not to include them. 
This policy applies to all initial (Type 1) applications submitted for 
receipt dates after October 1, 1998.
All investigators proposing research involving human subjects should read the 
"NIH Policy and Guidelines" on the Inclusion of Children as Participants in 
Research Involving Human Subjects that was published in the NIH Guide for 
Grants and Contracts, March 6, 1998, and is available at the following URL 
address: https://grants.nih.gov/grants/guide/notice-files/not98-024.html.
Investigators also may obtain copies of these policies from the program staff 
listed under INQUIRIES. Program staff may also provide additional relevant 
information concerning the policy.


All applications and proposals for NIH funding must self-contained within 
specified page limitations.  Unless otherwise specified in an NIH 
solicitation, internet addresses (URLs) should not be used to provide 
information necessary to the review because reviewers are under no obligation 
to view the Internet sites.  Revieweres are cautioned that their anonymity 
may be compromised when they directly access an Internet site.


The Public Health Service (PHS) is committed to achieving the health 
promotion and disease prevention objectives of "Healthy People 2010," a PHS-
led national activity for setting priority areas. This Request for 
Applications (RFA), “Spinal Muscular Atrophy, Amyotrophic Lateral Sclerosis, 
and Other Motor Neuron Disorders”, is related to one or more of the priority 
areas. Potential applicants may obtain a copy of "Healthy People 2010" at 


This program is described in the Catalog of Federal Domestic Assistance No. 
93.853. Awards are made under authorization of the Public Health Service Act, 
Title IV, Part A (Public Law 78-410, as amended by Public Law 99-158, 42 USC 
241 and 285) and administered under NIH grants policies and Federal 
Regulations 42 CFR 52 and 45 CFR Parts 74 and 92. This program is not subject 
to the intergovernmental review requirements of Executive Order 12372 or 
Health Systems Agency review.

The PHS strongly encourages all grant recipients to provide a smoke-free 
workplace and promote the non-use of all tobacco products. In addition, 
Public Law 103-227, the Pro-Children Act of 1994, prohibits smoking in 
certain facilities (or in some cases, any portion of a facility) in which 
regular or routine education, library, day care, health care, or early 
childhood development services are provided to children. This is consistent 
with the PHS mission to protect and advance the physical and mental health of 
the American people.

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