Accepted Manuscript Preface Michelle Wien , DrPH, RD PII:
S0197-4580(14)00356-X
DOI:
10.1016/j.neurobiolaging.2014.05.010
Reference:
NBA 8883
To appear in:
Neurobiology of Aging
Received Date: 20 November 2013 Accepted Date: 9 May 2014
Please cite this article as: Wien, M., Preface, Neurobiology of Aging (2014), doi: 10.1016/ j.neurobiolaging.2014.05.010. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Preface
1
RI PT
Michelle Wien, DrPH, RD1
Department of Nutrition
SC
Loma Linda University 24951 North Circle Drive
M AN U
Loma Linda, CA, USA 92350
Michelle Wien Department of Nutrition
EP
Loma Linda University
TE D
Corresponding Author:
AC C
24951 North Circle Drive
Loma Linda, CA, USA 92350 Telephone: 1-909-558-4598 Fax: 1-909-558-4095 Email: [email protected] 1
ACCEPTED MANUSCRIPT
The International Conference on Nutrition and the Brain was held on July 19-20, 2013 in Washington, D.C., and a subset of the conference proceedings are presented in this supplement. The conference served as a forum for researchers and health professionals to network, present
RI PT
and dialogue on emerging nutrition research that may prevent or delay the onset of neurological disorders, generate ideas for additional research hypotheses, and formulate a set of practical guidelines for clinicians to use with their patients. More than 500 attendees were present at the
SC
conference including physicians, researchers, dietitians, and nurses, and they enjoyed networking
M AN U
with each other during the formal presentations, brain-building boot-camp and social gatherings. The neurodegenerative disorders of the brain that were highlighted during the conference included Parkinson’s disease, multiple sclerosis (MS), and dementia, the latter being a clinical syndrome that results from an underlying pathology [e.g. Alzheimer’s disease (AD), vascular dementia, Lewy body and frontotemporal dementia]. The prevalence of dementia between 1980-
TE D
2009 among individuals aged ≥60 years in 21 Global Burden of Disease regions was estimated to be 35.6 million in 2010, and is predicted to reach 65.7 million in 2013 and 115.4 million in 2015 (Prince et al., 2013). The costs associated with dementia in 2010 were $604 billion globally, and
EP
the costs in 2030 are predicted to increase by 85% (Alzheimer’s Disease International, 2010).
AC C
The aforementioned neurological disorders are characterized by a progressive decline in cognition and contribute to both disability and dependence (Sousa et al., 2009; Sousa et al., 2010), which is prompting governments to address policymaking and planning in the context of their aging population and the emergence of a potential dementia epidemic. However, it is not only imperative for our health and social care systems to be prepared for the future trajectory of prevalence and costs; we must also seek ways to meet the needs of individuals currently living with dementia. 2
ACCEPTED MANUSCRIPT
Increasing evidence supports the importance of vascular factors (e.g. hypertension, diabetes, dyslipidemia, myocardial infarction) in the etiology of dementia and cognitive decline, and vascular lesions have been found in the majority of late onset cases of dementia and in
RI PT
approximately half of individuals with early onset dementia (Carotenuto et al., 2012). Therefore, first day of the conference featured globally recognized researchers who provided an update on the interplay of genes, dietary fats, vitamins and minerals in the context of influencing vascular
SC
factors that modulate the risk of developing neurological disorders. More specifically, experts discussed apolipoprotein E in the etiology of AD, dopamine’s role in diabetes and dementia, the
M AN U
influence of dietary fat and vitamin E on AD risk, copper dyshomeostasis in AD, and the role of iron in neurological disorders.
The second day of the conference included the topics of exercise on brain structure and functions, the role of sleep (e.g. amyloid-β diurnal pattern) in AD pathogenesis, and methods to
TE D
slow cognitive decline following chemotherapy. Additionally, experts discussed the role of specific B vitamins in reducing homocysteine to prevent brain atrophy and memory loss, and the
EP
use of a starch-based diet for the treatment of MS. The 2010 National Institute of Health’s State-of-the-Science-Conference on Preventing
AC C
Alzheimer’s Disease and Cognitive Decline report included the following statements “Evidence is insufficient to support the use of pharmaceutical agents or dietary supplements to prevent cognitive decline or Alzheimer’s disease. We recognize that a large amount of promising research is under way; these efforts need to be increased and added to by new understandings and innovations.” (National Institute of Health, 2010). Since individuals make decisions about dietary and lifestyle behaviors on a daily basis to reduce the risk of neurological disease, they 3
ACCEPTED MANUSCRIPT
must act on the best evidence available to them even when scientific consensus may not have yet been achieved. Therefore, as we wait for the findings from ongoing studies on antihypertensive medications, omega-3 fatty acids, physical activity, and cognitive engagement, a set of dietary
RI PT
and lifestyle guidelines for the prevention of AD was formulated by the experts and presented to the conference attendees for their immediate consideration and needs operating under the
SC
“precautionary principle.”
I would like to sincerely thank the conference presenters, members of the organizing and
M AN U
scientific planning committees, and the reviewers of the manuscripts. My hope is that the information provided in this supplement will expand the existing knowledge in the best practices for preventing and managing neurological disorders, and be a valuable resource for researchers
TE D
and health professionals to enrich their personal lives and to pass along to others.
Disclosure Statement
AC C
EP
The author declares no actual or potential conflicts of interest.
4
ACCEPTED MANUSCRIPT
References Alzheimer’s Disease International, 2010. World Alzheimer Report 2010. The Global Economic
http://www.alz.co.uk/research/files/WorldAlzheimerReport2010.pdf
RI PT
Impact of Dementia. Retrieved 10 Oct 2013, from
SC
Carotenuto, A., Rea, R., Colucci, L., Ziello, A.R., Molino, I., Carpi, S., Traini, E., Amenta, F., Fasanaro, A.M., 2012. Late and early onset dementia: What is the role of vascular factors? A
M AN U
retrospective study. J. Neurol. Sci. 322, 170-175.
National Institutes of Health, 2010. NIH Consensus and State-of-the-Science Statements. April 26-28, 2010. Retrieved 10 Oct 2013, from
TE D
http://consensus.nih.gov/2010/docs/alz/ALZ_Final_Statement.pdf
EP
Prince, M., Bryce, R., Albanese, E., Wimo, A., Ribeiro, W., Ferri, C.P., 2013. The global
75.e2.
AC C
prevalence of dementia: A systematic review and metaanalysis. Alzheimers Dement. 9, 63-
Sousa R.M., Ferri C.P., Acosta D., Albanese, E., Guerra, M., Huang, Y., Jacob, K.S., Jotheeswaran, A.T., Rodriguez, J.J., Pichardo, G.R., Rodriguez, M.C., Salas, A., Sosa, A.L., Williams, J., Zuniga, T., Prince, M., 2009. Contribution of chronic diseases to disability in
5
ACCEPTED MANUSCRIPT
elderly people in countries with low and middle incomes: a 10/66 Dementia Research Group
RI PT
population-based survey. Lancet. 374, 1821-1830.
Sousa R.M., Ferri C.P., Acosta D., Guerra, M., Huang, Y., Jacob, K., Jotheeswaran, A.,
Hernandez, M.A., Liu, Z., Pichardo, G.R., Rodriguez, J.J., Salas, A., Sosa, A.L., Williams, J.,
SC
Zuniga, T., Prince M., 2010. The contribution of chronic diseases to the prevalence of
dependence among older people in Latin America, China and India: A 10/66 Dementia Research
AC C
EP
TE D
M AN U
Group population-based survey. BMC Geriatr. Aug 6, 10:53. doi: 10.1186/1471-2318-10-53.
6
S0197-4580(14)00356-X
DOI:
10.1016/j.neurobiolaging.2014.05.010
Reference:
NBA 8883
To appear in:
Neurobiology of Aging
Received Date: 20 November 2013 Accepted Date: 9 May 2014
Please cite this article as: Wien, M., Preface, Neurobiology of Aging (2014), doi: 10.1016/ j.neurobiolaging.2014.05.010. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Preface
1
RI PT
Michelle Wien, DrPH, RD1
Department of Nutrition
SC
Loma Linda University 24951 North Circle Drive
M AN U
Loma Linda, CA, USA 92350
Michelle Wien Department of Nutrition
EP
Loma Linda University
TE D
Corresponding Author:
AC C
24951 North Circle Drive
Loma Linda, CA, USA 92350 Telephone: 1-909-558-4598 Fax: 1-909-558-4095 Email: [email protected] 1
ACCEPTED MANUSCRIPT
The International Conference on Nutrition and the Brain was held on July 19-20, 2013 in Washington, D.C., and a subset of the conference proceedings are presented in this supplement. The conference served as a forum for researchers and health professionals to network, present
RI PT
and dialogue on emerging nutrition research that may prevent or delay the onset of neurological disorders, generate ideas for additional research hypotheses, and formulate a set of practical guidelines for clinicians to use with their patients. More than 500 attendees were present at the
SC
conference including physicians, researchers, dietitians, and nurses, and they enjoyed networking
M AN U
with each other during the formal presentations, brain-building boot-camp and social gatherings. The neurodegenerative disorders of the brain that were highlighted during the conference included Parkinson’s disease, multiple sclerosis (MS), and dementia, the latter being a clinical syndrome that results from an underlying pathology [e.g. Alzheimer’s disease (AD), vascular dementia, Lewy body and frontotemporal dementia]. The prevalence of dementia between 1980-
TE D
2009 among individuals aged ≥60 years in 21 Global Burden of Disease regions was estimated to be 35.6 million in 2010, and is predicted to reach 65.7 million in 2013 and 115.4 million in 2015 (Prince et al., 2013). The costs associated with dementia in 2010 were $604 billion globally, and
EP
the costs in 2030 are predicted to increase by 85% (Alzheimer’s Disease International, 2010).
AC C
The aforementioned neurological disorders are characterized by a progressive decline in cognition and contribute to both disability and dependence (Sousa et al., 2009; Sousa et al., 2010), which is prompting governments to address policymaking and planning in the context of their aging population and the emergence of a potential dementia epidemic. However, it is not only imperative for our health and social care systems to be prepared for the future trajectory of prevalence and costs; we must also seek ways to meet the needs of individuals currently living with dementia. 2
ACCEPTED MANUSCRIPT
Increasing evidence supports the importance of vascular factors (e.g. hypertension, diabetes, dyslipidemia, myocardial infarction) in the etiology of dementia and cognitive decline, and vascular lesions have been found in the majority of late onset cases of dementia and in
RI PT
approximately half of individuals with early onset dementia (Carotenuto et al., 2012). Therefore, first day of the conference featured globally recognized researchers who provided an update on the interplay of genes, dietary fats, vitamins and minerals in the context of influencing vascular
SC
factors that modulate the risk of developing neurological disorders. More specifically, experts discussed apolipoprotein E in the etiology of AD, dopamine’s role in diabetes and dementia, the
M AN U
influence of dietary fat and vitamin E on AD risk, copper dyshomeostasis in AD, and the role of iron in neurological disorders.
The second day of the conference included the topics of exercise on brain structure and functions, the role of sleep (e.g. amyloid-β diurnal pattern) in AD pathogenesis, and methods to
TE D
slow cognitive decline following chemotherapy. Additionally, experts discussed the role of specific B vitamins in reducing homocysteine to prevent brain atrophy and memory loss, and the
EP
use of a starch-based diet for the treatment of MS. The 2010 National Institute of Health’s State-of-the-Science-Conference on Preventing
AC C
Alzheimer’s Disease and Cognitive Decline report included the following statements “Evidence is insufficient to support the use of pharmaceutical agents or dietary supplements to prevent cognitive decline or Alzheimer’s disease. We recognize that a large amount of promising research is under way; these efforts need to be increased and added to by new understandings and innovations.” (National Institute of Health, 2010). Since individuals make decisions about dietary and lifestyle behaviors on a daily basis to reduce the risk of neurological disease, they 3
ACCEPTED MANUSCRIPT
must act on the best evidence available to them even when scientific consensus may not have yet been achieved. Therefore, as we wait for the findings from ongoing studies on antihypertensive medications, omega-3 fatty acids, physical activity, and cognitive engagement, a set of dietary
RI PT
and lifestyle guidelines for the prevention of AD was formulated by the experts and presented to the conference attendees for their immediate consideration and needs operating under the
SC
“precautionary principle.”
I would like to sincerely thank the conference presenters, members of the organizing and
M AN U
scientific planning committees, and the reviewers of the manuscripts. My hope is that the information provided in this supplement will expand the existing knowledge in the best practices for preventing and managing neurological disorders, and be a valuable resource for researchers
TE D
and health professionals to enrich their personal lives and to pass along to others.
Disclosure Statement
AC C
EP
The author declares no actual or potential conflicts of interest.
4
ACCEPTED MANUSCRIPT
References Alzheimer’s Disease International, 2010. World Alzheimer Report 2010. The Global Economic
http://www.alz.co.uk/research/files/WorldAlzheimerReport2010.pdf
RI PT
Impact of Dementia. Retrieved 10 Oct 2013, from
SC
Carotenuto, A., Rea, R., Colucci, L., Ziello, A.R., Molino, I., Carpi, S., Traini, E., Amenta, F., Fasanaro, A.M., 2012. Late and early onset dementia: What is the role of vascular factors? A
M AN U
retrospective study. J. Neurol. Sci. 322, 170-175.
National Institutes of Health, 2010. NIH Consensus and State-of-the-Science Statements. April 26-28, 2010. Retrieved 10 Oct 2013, from
TE D
http://consensus.nih.gov/2010/docs/alz/ALZ_Final_Statement.pdf
EP
Prince, M., Bryce, R., Albanese, E., Wimo, A., Ribeiro, W., Ferri, C.P., 2013. The global
75.e2.
AC C
prevalence of dementia: A systematic review and metaanalysis. Alzheimers Dement. 9, 63-
Sousa R.M., Ferri C.P., Acosta D., Albanese, E., Guerra, M., Huang, Y., Jacob, K.S., Jotheeswaran, A.T., Rodriguez, J.J., Pichardo, G.R., Rodriguez, M.C., Salas, A., Sosa, A.L., Williams, J., Zuniga, T., Prince, M., 2009. Contribution of chronic diseases to disability in
5
ACCEPTED MANUSCRIPT
elderly people in countries with low and middle incomes: a 10/66 Dementia Research Group
RI PT
population-based survey. Lancet. 374, 1821-1830.
Sousa R.M., Ferri C.P., Acosta D., Guerra, M., Huang, Y., Jacob, K., Jotheeswaran, A.,
Hernandez, M.A., Liu, Z., Pichardo, G.R., Rodriguez, J.J., Salas, A., Sosa, A.L., Williams, J.,
SC
Zuniga, T., Prince M., 2010. The contribution of chronic diseases to the prevalence of
dependence among older people in Latin America, China and India: A 10/66 Dementia Research
AC C
EP
TE D
M AN U
Group population-based survey. BMC Geriatr. Aug 6, 10:53. doi: 10.1186/1471-2318-10-53.
6
