Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5264_Библиотеки_им_академика_М_И_Перельмана.pdf
194
Plant-based Foods and their Implications in Brain Health
82. Kovacs GG, Ferrer I, Grinberg LT, Alafuzoff I, Attems J, Budka H, Cairns NJ, Crary JF, Duyckaerts
C, Ghetti B, et al. Acta Neuropathol, 131: 87– 102, (2016).
83. Schultz C, Ghebremedhin E, Del Tredici K, Rub U, Braak H. Neurobiol Aging, 25: 397– 405, (2004).
84. Williams DR, Lees AJ. Lancet Neurol, 8: 270– 279, (2009).
85. Dickson DW, Ahmed Z, Algom AA, Tsuboi Y, Josephs KA. Curr Opin Neurol, 23: 394– 400, (2010).
86. Arai T, Ikeda K, Akiyama H, Nonaka T, Hasegawa M, Ishiguro K, Iritani S, Tsuchiya K, Iseki E,
Yagishita S, et al. Ann Neurol, 55: 72– 79, (2004).
87. Rebeiz JJ, Kolodny EH, Richardson EP Jr. Arch Neurol, 18: 20– 33, (1968).
88. Gibb WR, Luthert PJ, Marsden CD. Brain, 112: 1171– 1192, (1989).
89. Ikeda K, Akiyama H, Haga C, Kondo H, Arima K, Oda T. Neurosci Lett, 174: 157– 159, (1994).
90. Feany MB, Dickson DW. Am J Pathol, 146: 1388– 1396, (1995).
91. Dickson DW, Bergeron C, Chin SS, Duyckaerts C, Horoupian D, Ikeda K, Jellinger K, Lantos PL,
Lippa CF, Mirra SS, et al. J Neuropathol Exp Neurol, 61: 935– 946, (2002).
92. Spillantini MG, Goedert M. Lancet Neurol, 12: 609– 622, (2013).
93. Armstrong MJ, Litvan I, Lang AE, Bak TH, Bhatia KP, Borroni B, Boxer AL, Dickson DW, Grossman
M, Hallett M, et al. Neurology, 80: 496– 503, (2013).
94. Hassan A, Whitwell JL, Boeve BF, Jack CR Jr, Parisi JE, Dickson DW, Josephs KA. Parkinsonism
Relat Disord 16: 208– 214, (2010).
95. Kouri N, Whitwell JL, Josephs KA, Rademakers R, Dickson DW. Nat Rev Neurol, 7: 263– 272,
(2011).
96. Ueda K, Fukushima H, Masliah E, Xia Y, Iwai A, Yoshimoto M, Otero DA, Kondo J, Ihara Y, Saitoh
T. Proc Natl Acad Sci, 90: 11282– 11286, (1993).
97. Sudhof TC, Rizo J. Cold Spring Harb Perspect Biol, 3: a005637, (2001).
98. Polymeropoulos MH, Lavedan C, Leroy E, Ide SE, Dehejia A, Dutra A, Pike B, Root H, Rubenstein
J, Boyer R, et al., Science, 276: 2045– 2047, (1997).
99. Spillantini MG, Schmidt ML, Lee VM, Trojanowski JQ, Jakes R, Goedert M. Nature, 388: 839– 840,
(1997).
100. Lantos PL. J Neuropathol Exp Neurol, 57: 1099– 1111, (1998).
101. Irizarry MC, Growdon W, Gomez- Isla T, Newell K, George JM, Clayton DF, Hyman BT. J
Neuropathol Exp Neurol, 57: 334– 337, (1998).
102. Leverenz JB, Umar I, Wang Q, Montine TJ, McMillan PJ, Tsuang DW, Jin J, Pan C, Shin J, Zhu D,
et al. Brain Pathol, 17: 139– 145, (2007).
103. Galvin JE, Lee VM, Baba M, Mann DM, Dickson DW, Yamaguchi H, Schmidt ML, Iwatsubo T,
Trojanowski JQ. Ann Neurol, 42: 595– 603, (1993).
104. Kuusisto E, Parkkinen L, Alafuzoff I. J Neuropathol Exp Neurol, 62: 1241– 1253, (2003).
105. Ishizawa T, Mattila P, Davies P, Wang D, Dickson DW. J Neuropathol Exp Neurol, 62: 389– 397,
(2003).
106. Dugger BN, Dickson DW. Acta Neuropathol, 120: 633– 639, (2010).
107. Dickson DW. Curr Opin Neurol, 14: 423– 432, (2001).
108. Kosaka K, Yoshimura M, Ikeda K, Budka H. Clin Neuropathol, 3: 185– 192, (1994).
109. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien JT, Feldman H, Cummings J, Duda JE, Lippa
C, Perry EK, et al. Neurology, 65: 1863– 1872, (2005).
110. Braak H, Del Tredici K, Rub U, de Vos RA, Jansen Steur EN, Braak E., Neurobiol Aging, 24: 197–
211, (2003).
111. Alafuzoff I, Ince PG, Arzberger T, Al- Sarraj S, Bell J, Bodi I, Bogdanovic N, Bugiani O, Ferrer I,
Gelpi E, et al. Acta Neuropathol, 117: 635– 652, (2009a).
112. Uchikado H, Lin WL, DeLucia MW, Dickson DW. J Neuropathol Exp Neurol, 65: 685– 697, (2006b).
113. Beach TG, Adler CH, Lue L, Sue LI, Bachalakuri J, Henry- Watson J, Sasse J, Boyer S, Shirohi S,
Brooks R, et al. Acta Neuropathol, 117: 613– 634, (2009).
114. Toledo JB, Gopal P, Raible K, Irwin DJ, Brettschneider J, Sedor S, Waits K, Boluda S, Grossman M,
Van Deerlin VM, et al. Acta Neuropathol, 131: 393– 409, (2016).
115. Halliday G, Hely M, Reid W, Morris J, Acta Neuropathol,115: 409– 415, (2008).
116. Dugger BN, Adler CH, Shill HA, Caviness J, Jacobson S, Driver- Dunckley E, Beach TG.
Parkinsonism Relat Disord, 20: 525– 529, (2014a).
195
Marine Plant Species: Nutritional and Medicinal Value
117. Dugger BN, Serrano GE, Sue LI, Walker DG, Adler CH, Shill HA, Sabbagh MN, Caviness JN,
Hidalgo J, Saxon- Labelle M, et al, J Parkinsons Dis, 2: 57– 65, (2012).
118. Ratti A, Buratti E. J Neurochem, 138: 95– 111, (2016).
119. Neumann M, Sampathu DM, Kwong LK, Truax AC, Micsenyi MC, Chou TT, Bruce J, Schuck T,
Grossman M, Clark CM, et al. Science, 314: 130– 133, (2006).
120. Amador- Ortiz C, Lin WL, Ahmed Z, Personett D, Davies P, Duara R, Graff- Radford NR, Hutton ML,
Dickson DW. Ann Neurol, 61: 435– 445, (2007).
121. Hu WT, Josephs KA, Knopman DS, Boeve BF, Dickson DW, Petersen RC, Parisi JE. Acta
Neuropathol, 116: 215– 220, (2008).
122. Josephs KA, Murray ME, Whitwell JL, Parisi JE, Petrucelli L, Jack CR, Petersen RC, Dickson DW.
Acta Neuropathol, 127: 441– 450, (2014).
123. Fujishiro H, Uchikado H, Arai T, Hasegawa M, Akiyama H, Yokota O, Tsuchiya K, Togo T, Iseki E,
Hirayasu Y. Acta Neuropathol, 117: 151– 158, (2009).
124. Arnold SJ, Dugger BN, Beach TG. 2013. Acta Neuropathol, 126: 51– 57, (2013).
125. Lomen- Hoerth C, Anderson T, Miller B. Neurology, 59: 1077– 1079, (2002).
126. Ince PG, Highley JR, Kirby J, Wharton SB, Takahashi H, Strong MJ, Shaw PJ. 2011. Acta
Neuropathol, 122: 657– 671, (2011).
127. Sangnoi Y, Sakulkeo O, Yuenyongsawad S, Kanjana- opas A, Ingkaninan K, Plubrukarn A,
Suwanborirux K. Mar. Drugs, 6, 578– 586, (2008).
128. Le TC, Katila N, Park S, Lee J, Yang I, Choi H, Choi D- Y, Nam S- J. Bioorg. Med. Chem. Lett., 2020,
30, 127145, (2020).
129. Williams PG, Yoshida WY, Moore RE, Paul VJ. J. Nat. Prod., 66, 1006– 1009, (2003).
130. Liu Y, Zhang W, Li L, Salvador LA, Chen T, Chen W, Felsenstein KM, Ladd TB, Price AR, Golde
TE. J. Med. Chem., 55, 10749– 10765, (2012).
131. Al- Awadhi FH, Ratnayake R, Paul VJ, Luesch H, Tasiamide F. Bioorg. Med. Chem., 24, 3276– 3282,
(2016).
132. Nachtigall J, Schneider K, Bruntner C, Bull AT, Goodfellow M, Zinecker H, Imhoff JF, Nicholson G,
J. Antibiot., 64, 453– 457, (2011).
133. Kim TK, Hewavitharana AK, Shaw PN, Fuerst JA. Appl. Environ. Microbiol., 72, 2118– 2125,
(2006).
134. Kilic Ü, Kilic E, Lingor P, Yulug B, Bähr M. Acta Neuropathol. Finder V.H, Glockshuber R.
Neurodegener. Dis., 4, 13– 27, (2007).
135. Alvarino R, Alonso E, Lacret R, Oves- Costales D, Genilloud O, Reyes F, Alfonso A, Botana LM.
Mol. Pharm., 16, 1456– 1466, (2019).
136. Cao J, Li X- M, Meng L- H, Konuklugil B, Li X, Li H- L, Wang B- G. Bioorg. Chem., 90, 103030,
(2019).
137. He J- B, Ji Y- N, Hu D- B, Zhang S, Yan H, Liu X- C, Luo H- R, Zhu H- J. Tetrahedron Lett., 55, 2684–
2686, (2014).
138. Huang H, Feng X, Xiao ZE, Liu L, Li H, Ma L, Lu Y, Ju J, She Z, Lin Y. J. Nat. Prod., 74, 997– 1002,
(2011).
139. Yang W- C, Bao H- Y, Liu Y- Y, Nie Y- Y, Yang J- M, Hong P- Z, Zhang Y. Molecules, 23, 2245, (2018).
140. Wu B, Ohlendorf B, Oesker V, Wiese J, Malien S, Schmaljohann R, Imhoff JF. Mar. Biotechnol., 17,
110– 119, (2015).
141. Chen S, Liu H, Ye W, Li S, Li D, Liu Z, Zhang. Tetrahedron, 76, 131066, (2020).
142. Li K- L, Dai Y, She J- L, Zeng Y- B, Dai H- F, Ou S- L, Zhou X- F, Liu Y- H. J. Asian Nat. Prod. Res.,
1– 8, (2021).
143. Qiao MF, Ji NY, Miao FP, Yin X. Magn. Reson. Chem., 49, 366– 369, (2011).
144. An C- L, Kong F- D, Li Y, Ma Q- Y, Xie Q- Y, Yuan J- Z, Zhou L- M, Dai H- F, Yu Z- F, Zhao Y- X.
J. Asian Nat. Prod. Res., 23, 1– 6, (2020).
145. Bunbamrung N, Intaraudom C, Dramae A, Komwijit S, Laorob T, Khamsaeng S, Pittayakhajonwut
P. Tetrahedron, 76, 131496, (2020).
146. Nong X- H, Wang Y- F, Zhang X- Y, Zhou M- P, Xu X- Y, Qi S- H. Mar. Drugs, 12, 6113– 6124, (2014).
147. Ding B, Wang Z, Huang X, Liu Y, Chen W, She Z. Nat. Prod. Res., 30, 2805– 2812, (2016).
148. Qiao MF, Ji NY, Miao FP, Yin XL. Magn. Reson. Chem., 49, 366– 369, (2011).
196
Plant-based Foods and their Implications in Brain Health
149. Wu B, Wiese J, Schmaljohann R, Imhoff JF. Mar. Drugs, 14, 204, (2016).
150. Schulz D, Ohlendorf B, Zinecker H, Schmaljohann R, Imhoff JF. J. Nat. Prod., 74, 99– 101, (2011).
151. Lin Y, Wu X, Feng S, Jiang G, Luo J, Zhou S, Vrijmoed LLP, Jones EBG, Krohn K, Steingröver K.
et al., J. Org. Chem., 66, 6252– 6256, (2001).
152. Kannan RR, Aderogba MA, Ndhlala, AR, Stirk WA, Van Staden J. Food Res. Int., 54, 1250– 1254,
(2013).
153. Lee BH, Choi BW, Lee SY. Ocean Polar Res., 39, 45– 49, (2017).
154. Paudel P, Seong SH, Zhou Y, Park HJ, Jung HA, Choi JS. ACS Omega, 4, 12259– 12270, (2019).
155. Gonçalves KG, da Silva LL, Soares AR, Romeiro NC. Algal Res., 52, 102130, (2020).
156. Syad AN, Devi KP. Neurol. Res., 37, 14– 22, (2015).
157. Castro- Silva E, Bello M, Hernández- Rodríguez M, Correa- Basurto J, Murillo- Alvarez J, Rosales-
Hernandez M, Muñoz- Ochoa, MJ. Biomol. Struct. Dyn., 37, 3259– 3268, (2018).
158. Jung HA, Ali MY, Choi RJ, Jeong, HO, Chung, HY, Choi JS. Food Chem. Toxicol., 89, 104– 111,
(2016).
159. Miyashita K, Function of marine carotenoids. Yoshikawa, T., Ed.; Forum Nutr. Basel: Karger,
Switzerland, 61, 136– 146, (2009).
160. Lin J, Huang L, Yu J, Xiang S, Wang J, Zhang J, Yan X, Cui W, He S, Wang Q. Mar. Drugs, 14, 67,
(2016).
161. Choi BW, Ryu G, Park SH, Kim ES, Shin J, Roh SS, Shin HC, Lee BH. Phytother. Res., 21, 423– 426,
(2007).
162. Seong SH, Ali MY, Kim H- R, Jung HA, Choi JS, Med. Chem., 25, 3964– 3970, (2017).
163. Tello E, Castellanos L, Arevalo- Ferro C, Duque C, J. Nat. Prod., 72, 1595– 1602, (2009).
164. Food
Res. Int., 77, 118– 124, (2015).
165. Mohibbullah M, Haque MN, Khan MNA, Park I- S, Moon IS, Hong, Y- K, J. Appl. Phycol., 30, 3243–
3252, (2018).
166. Zhang L, Wang H, Fan Y, Gao Y, Li X, Hu Z, Ding K, Wang Y, Wang X. Sci. Rep., 7, 46763, (2017).
167. Alghazwi M, Smid S, Karpiniec S, Zhang W. Int. J. Biol. Macromol., 122, 255– 264, (2019).
168. Lee JK, Byun H- G. “A novel BACE inhibitor isolated from Eisenia bicyclis exhibits neuroprotective
Fish. Aquat. Sci., 21, 38, (2018).
169. Liu D- Q, Mao S- C, Zhang H- Y, Yu X- Q, Feng M- T, Wang B, Feng L- H, Guo Y- W. Fitoterapia, 91,
15– 20, (2013).
170. Seong SH, Paudel P, Jung HA, Choi JS. Mar. Drugs, 17, 600, (2019).
171. Yang P, Liu D- Q, Liang T- J, Li J, Zhang H- Y, Liu A- H, Guo Y- W, Mao S- C. Bioorg. Med. Chem., 23,
38– 45, (2015).
172. Wang J, Zheng J, Huang C, Zhao J, Lin J, Zhou X, Naman C.B.;Wang, N, Gerwick WH, Wang Q,
et al. Neurosci., 9, 1349– 1356, (2018).
173. Hielscher- Michael S, Griehl C, Buchholz M, Demuth H- U, Arnold N. , Wessjohann LA. Mar. Drugs,
14, 203, (2016).
174. Liu H, Gu L. J. Agric. Food Chem., 60, 1326– 1334, (2012).
175. Vanderlei ESO, Patoilo KKNR, Lima NA, Lima APS, Rodrigues JAG, Silva LMCM, Lima MEP,
Lima V, Benevides NMB. Int. Immunopharmacol., 10, 1113– 1118, (2010).
176. Liu X, Shibata T, Hisaka S, Osawa T, Brain Res., 1254, 18– 27, (2009).
177. Fakhri S, Yosifova Aneva I, Farzaei MH, Sobarzo- Sánchez E. Molecules, 24, 2640, (2019).
178. Ikeda Y, Tsuji S, Satoh A, Ishikura M, Shirasawa T, Shimizu T. J. Neurochem., 107, 1730– 1740,
(2008).
179. Souza RB, Frota AF, Silva J, Alves C, Neugebauer AZ, Pinteus S, Rodrigues JAG, Cordeiro EMS, de
Almeida RR, Pedrosa R, et al. Int. J. Biol. Macromol., 112, 1248– 1256, (2018).
180. Luo D, Zhang Q, Wang H, Cui Y, Sun Z, Yang J, Zheng Y, Jia J, Yu F, Wang X. et al., Eur. J. Pharmacol.,
617, 33– 40, (2009).
181. Celikler S, Vatan O, Yildiz G, Bilaloglu R. Food. Chem. Toxicol., 47, 796– 801, (2009).
182. Hannan MA, Dash R, Haque MN, Mohibbullah M, Sohag AAM, Rahman MA, Uddin MJ, Alam M,
Moon IS. Mar. Drugs, 18, 347, (2020).
183. Jiang Z, Hama Y, Yamaguchi K, Oda T. J. Biochem, 151, 65– 74, (2011).
184. Shang Q, Jiang H, Cai C, Hao J, Li G, Yu G. Carbohydr. Polym., 179, 173– 185, (2018).
197
Marine Plant Species: Nutritional and Medicinal Value
185. Zargarzadeh M, Amaral AJ, Custódio CA, Mano JF. Carbohydr. Polym., 232, 115774, (2020).
186. Liu X- Y, Liu D, Lin G- P, Wu Y- J, Gao L- Y, Ai C, Huang Y- F, Wang M- F, El- Seedi HR, Chen X- H,
et al., Int. J. Biol. Macromol, 139, 342– 351, (2019).
187. Tsolaki M. Hell. J. Nucl. Med., 22, 82– 94, (2019).
188. Shimizu H, Koyama T, Yamada S, Lipton SA, Satoh T, Zonarol. Biochem. Biophys. Res. Commun.,
457, 718– 722, (2015).
189. Wozniak M, Bell T, Dénes Á, Falshaw R, Itzhaki R. Int. J. Biol. Macromol, 74, 530– 540, (2015).
190. Yoon NY, Lee SH, Yong L, Kim SK. J. Funct. Foods, 1, 331– 335, (2009).
191. Bauer S, Jin W, Zhang F, Linhardt R.J. Mar. Drugs, 19, 89, (2021).
192. Rocha De Souza MC, Marques CT, Guerra Dore CM, Ferreira Da Silva, FR, Oliveira Rocha HA,
Leite EL. J. Appl. Phycol., 19, 153– 160, (2007).
198
DOI: 10.1201/9781003300502-9
9
Walnut (Juglans regia L.)
as Brain Food
Atanu Bhattacharjee, Akula Ramakrishna, and
Kunal Bhattacharya
9.1 INTRODUCTION
many nations. The prevalence of neurodegenerative illnesses has increased as a result of this demo-
graphic transition. It has been estimated that over 35 million folks across the globe are suffering
from dementia, and approximately 7 million Americans have been given a diagnosis of dementia or
another neurologic condition (1
disorders, which also places a heavy economic liability on both victims and their relatives. Due to
the synchronization of brain cells, the progression of the disease converted from mild to moderate
to extreme within 5– 9 years (2).
buildup of harmful proteins are all factors in neurodegenerative disorders. These elements set off
a chain reaction of changed chemical events that damage or kill brain cells as we age. Memory,
individual cell damage. Neurodegenerative illnesses like Alzheimer's disease (AD), Parkinson's
disease, dementia etc., are eventually caused by these cellular changes (2,3). Free radical- induced
neurodegenerative disorders. Therefore, the primary goal is to provide systemic defence against
shield to the brain to maintain its healthy status and function smoothly without hiccups.
Neurodegeneration may be halted or prevented by dietary changes. A large community- based,
case- control cohort study involving 194 AD patients and 1790 non- AD patients found that the
4).
In a cohort trial with 1367 patients > 65 years of age, a related inquiry demonstrated a lower risk of
5). The Mediterranean diet has been shown
to reduce the risk of dementia and death in AD patients, according to a few other research. These
studies also highlight the critical importance of fruit and nut bioactive components for maintaining
cognitive function (6,7).
Linoleic acid (LA; 18:2n6), - linolenic acid (ALA; 18:3n3), and other polyphenolics,
phytosterols, and micronutrients are abundant in English walnuts (Juglans regia L.) (8,9).
Experiments have demonstrated that feeding old animals walnut supplements can enhance their
memory, cognition, and motor performance. Despite the fact that the majority of this research
has focused on walnuts’ high PUFA content, walnuts’ considerable polyphenol content also
(10,11). This review discusses recent studies on the effects of dietary walnuts on brain health,
cognition, and motor performance.
199
Walnut (Juglans regia L.) as Brain Food
9.2 PHYTOCONSTITUENTS OF WALNUT
In terms of weight, walnuts have around 65% fat. Walnuts, like other nuts, get the majority of their
energy from fat. They are, therefore, a calorie- dense, high- energy food. Walnuts are high in fat and
calories, but research shows that when they are substituted for other items in the diet, they do not
raise the risk of obesity. Triacylglycerols make up the majority of the oil’s components; free fatty
acids, diacylglycerols, monoacylglycerols, sterols, sterol esters, and phosphatides are only trace
linolenic (18:3) fatty acids. Linoleic acid, an omega- 6 fatty acid, is the most prevalent. They also
% of the total fat content is made up of this. Actually, the only nuts with considerable ALA con-
tent are walnuts (13,14,15). ALA is thought to be particularly advantageous for heart health (16).
chain omega- 3 fatty acids EPA and DHA, which have been associated with a number of health
advantages, are precursors of ALA (17, 18).
9.2.1 amino aCidS
Amino acids present in walnuts are a great source of protein required for a healthy diet. According
to reports, walnuts have a protein concentration that ranges from 13.6 to 18.1 gm per 100 g of DM.
arginine may be turned into nitric oxide, a powerful vasodilator that can prevent platelet adhe-
sion and aggregation, the high quantities of arginine in walnuts have already been recognized as a
in- vivo (20, 21).
9.2.2 dietary fibre and phytoSterolS
g dry matter in different varieties. A subsequent amount of phytosteroids were detected in walnuts.
It was reported that moderate intake of walnut powder reduces serum total cholesterol in vivo via
decrease in their absorption (22).
9.2.3 mineralS and vitaminS
Walnuts are high in a variety of vitamins and minerals (Table 9.1), including:
9.2.4 vitamin e
Walnuts are high in a kind of vitamin E known as α- tocopherol. Vitamin E has strong antioxidant
properties and helps to prevent lipid peroxidation (23).
9.2.5 vitamin b6
This vitamin may help to boost the immune system and maintain neurological function. Anaemia
can be caused by a lack of vitamin B6 (23).
9.2.6 vitamin b9
Folic acid, often known as folate, serves a variety of biological activities. A lack of folic acid during
pregnancy may result in birth abnormalities (23).
200
Plant-based Foods and their Implications in Brain Health
9.2.7 mineralS
Copper: Copper is an essential trace element in the human body. Copper serves as a prosthetic
group that is permanently bound to many critical enzymes involved in the creation of ATP, iron
metabolism, neuropeptide activation, and neurotransmitters formation. It also plays a crucial role to
maintain catecholamine balance, myelination, and signal transduction in between two neurons in the
CNS. It has been reported that abnormal copper-protein interactions may generate free radicals via
the Haber-Weiss reaction resulting in mitochondrial damage, DNA breakage, and neuronal injury
which may be associated with neurological disorders like depression, Alzheimer’s etc. (25).
Phosphorus: Phosphorus, a mineral found mostly in bones, accounts for around 1% of our total
weight. It serves several roles in the organism (24).
Manganese: The largest concentrations of this trace element are found in nuts, whole grains,
fruits, and vegetables. Other plant compounds in walnuts contain a rich variety of bioactive plant
components. They are extremely high in antioxidants, which are concentrated in the thin, brown
skin (24).
Ellagic acid derivatives: Ellagic acid is a polyphenolic compound. This antioxidant is abundant in
walnuts, as are other related chemicals such as ellagitannins. Ellagic acid may lower the risk of heart
disease and aid in the suppression of cancer development (26).
Catechin:
heart health (6).
Melatonin: It is a tryptophan base and neurohormone aiding in the regulation of the body clock. It
is also a potent antioxidant, which may lower the risk of heart disease (27,28).
9.3 THERAPEUTIC BENEFITS OF BRAIN FOOD
9.3.1 Cognitive benefit
In a clinical trial with 64 human volunteers, it was observed that the administration of walnuts (10
gm/ day; 8 weeks) improves verbal reasoning abilities and motor function by 11.2 %. This effect may
be associated with antioxidant potential of the fruit (28, 29).
TABLE 9.1
Vitamins and minerals essential for healthy brain cells
B Complex Necessary for the production of neurotransmitters, neuronal cell membranes,
References
Vitamin E Natural antioxidant and protect neurons via reducing oxidative stress and
free radical scavenging activity
23
Magnesium and Calcium Regulation of nerve impulse transmission between brain cells; Ca
2+
a nerve terminal induces neurotransmitter release
24
Zinc Prosthetic element for enzyme activation; structural component of
neuropeptides in brain cell
25
Iron Carrier of oxygen to the brain cells essential for their survival and vitality;
helps in neurotransmitter synthesis
25
Phytonutrients (such as
Neuro- protective function through its role as an antioxidant 27,28
201
Walnut (Juglans regia L.) as Brain Food
9.3.2 ageing and metaboliC effeCtS on brain health
It has been postulated that the human brain consumes a higher amount of oxygen comparatively
as it requires enhanced metabolic reactions. These physiological responses lead to generate dis-
proportionate amounts of reactive oxygen species (ROS) and reactive nitrogen species (RNS).
The generated ROS and RNS are scavenged by antioxidant enzymes like oxydo- reductase, SOD,
catalase etc. extrinsically, whereas intrinsic amino acids act as molecular quenchers at the cellular
level and thereby maintain the haemostatics (30,31,32). Another theory depicts oxidative stress
various cognitive and behavioural abilities (33, 34).
Learning is the acquisition of information and skills, and subsequent retention of that informa-
tion is known as memory. Thus, cognition is a process of storing a sequence of information in a
systematic manner by which one becomes aware of one's surroundings, objects and thoughts (35).
During the process of learning and memory formation, the brain undergoes various physical and
chemical changes known as synaptic plasticity. It involves various signal transduction pathways
and induction of gene expression, which results in the formation of new synapses between nerve
cells (36). The main characteristic of memory formation in animals and human beings is its pro-
gression from a short- lived liable form to a long- lasting stable form (37). This process undergoes a
continuous remodelling with time and new experiences. Principally, the memory process consists
of three different stages, viz. registration, consolidation and retrieval. Registration is the process
of sensory perception and the ability to act on the information perceived (behavioural responses),
which involves a change in brain activity (electrical and electrochemical) and is referred to as short-
term memory. Consolidation is the process of conversion of registered short- term information to
long- term memory, which involves physicochemical changes in neuronal networks (38,39). The
stored information is made accessible by the process known as retrieval (Figure 9.1).
The consolidation hypothesis postulates that memory storage proceeds through temporally distinct
phases, each disrupted by a subset of agents like electro- convulsive shock, etc. The retrieval
hypothesis postulates that amnesic agents like scopolamine, etc., disrupt memory recall rather than
storage, as the effect of these agents diminishes over time, resulting in the appearance of normal
FIGURE 9.1 Multiple stages of cognition process.
202
Plant-based Foods and their Implications in Brain Health
memory retention (40). The consolidation of information is mediated by limbic structures, with the
hippocampal formation playing a vital role in the memory process (41). There are two major pathways
involved in the mechanism of learning and memory process viz. Papez pathway and cortical pathway.
The Papez circuit is a neural circuit connecting the hypothalamus to the limbic lobe and controls emo-
tional aspects of behaviour. The Papez circuit goes through the following neural pathway:
The second pathway leading from the cortical association areas via cingulate gyrus to the hippo-
campus via thalamic nucleus and enables information to be stored, presumably allowing it to rever-
berate for some time for body response (Figure 9.2) (42).
Memory function is vulnerable to a variety of pathological conditions, including
neurodegenerative diseases like AD. Dementia, an age- related mental problem, is a characteristic
symptom of AD (43).
It has been reported that the composition of PUFA decreases in neuronal membranes during
ageing, which causes neuronal function to directly hamper neuronal networking symmetry. Due to a
decline in PUFA level, neuronal functions are affected, which ultimately leads to altered neurosignal
transmission within the brain. Walnut is a rich source of PUFA and therefore may increase PUFAs
content in brain neuronal cells and thereby maintain healthy status of brain neuronal cells (44, 45).
9.4 BRAIN CELL PROTECTIVE ACTIVITY OF WALNUT PHYTOCHEMICALS:
IN- VITRO STUDIES
Walnuts are a rich source of nutrients and bioactive phytochemicals. It contains a high amount of
ω- 3- fatty acids and other PUFAs (Table 9.2 and Figure 9.3). Collectively they boost brain health and
function by providing nourishment and free radical scavenging property (46,47).
In human liver cells, α- Lenoleic acid present in walnuts is converted to DHA through enzyme-
mediated sequential desaturation process (Figure 9.1). Both EPA and DHA are vital for brain health
because they not only reduce oxidative stress and modify immunological function but also preserve
neuronal membrane integrity, gene expression, and neurogenesis (49).
The polyphenolic compounds, vitamin E, carotenoids, and minerals, along with PUFAs, provide
defence against ROS/ RNS- induced toxicity and protection through inhibition of LPO via increased
plasma antioxidant capacity. Polyphenols promote neuronal calcium homeostasis in the striatum
and hippocampus, regions of the brain crucial for primary and secondary memory functions (50).
FIGURE 9.2 Major pathways of learning and memory process.
203
Walnut (Juglans regia L.) as Brain Food
Walnut is enriched with tryptophan base melatonin. Endogenous melatonin is a primary hormone
to regulate circadian rhythms (51, 52).
It also possesses antioxidant and neuro- protective roles in AD. Melatonin plays a protective role in
Due to melatonin- rich content, intake of walnuts increased blood melatonin concentrations, thereby
showing prophylactic activity against neural damage in the brain and subsequently preventing the
early stages of AD (53,54,55).
-
matory mediators like NO production and TNF- α
protected against LPS- induced loss of calcium recovery (56). Another similar type of study also
FIGURE 9.3
TABLE 9.2
Fatty acids of walnuts
Fatty acid Amount/ 100g
Lenileic acid (LA) 38 g
α-Lenileic acid (ALA) 9.0 g
Saturated fatty acid (palmitic acid) 4.4 g
Monounsaturated fatty acid (oleic acid) 8.7 g
Polyunsaturated fatty acid (oleic acid) 20.4 g