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Regional specificity of alterations in NGF, BDNF and NT-3 levels in Alzheimerʼs disease
Abstract
Using two-site enzyme immunoassays (EIAs), we measured the levels of neurotrophins, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) simultaneously in three brain regions (motor cortex, dentate gyrus and entorhinal cortex) of patients with Alzheimer's disease (AD) and control individuals. Significant differences between the neurotrophin levels of these two groups were found in the different brain regions depending on the neurotrophin. The NGF level in the dentate gyrus of AD patients was higher, whereas the BDNF level in the entorhinal cortex and the NT-3 level in the motor cortex were lower than the corresponding control levels. These results indicate that protein levels of individual neurotrophins in different brain regions are affected differently by AD, and such differential changes may contribute to the complex pathology of AD.
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“A reduced level of BDNF has been found in patients affected by neurodegenerative diseases such as Parkinson’s, Huntington’s and Alzheimer’s disease as well as in mild cognitive impairment, the latter being a prodromal stage of AD, characterized by a slight decline of cognitive abilities including memory, thinking and judging skills [242,243,244,245].”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [244]
In the citing paper
“Furthermore, amounts of BDNF protein are reduced in the entorhinal cortex and hippocampus in Alzheimer’s disease7–9.”
From Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer's disease (2009) · cites this paper as [7]
In the citing paper
“Notably, the concentrations of BDNF decline in the entorhinal cortex and hippocampus in Alzheimer’s disease7–9”
From Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer's disease (2009) · cites this paper as [7]
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“Moreover, BDNF levels are reduced in the entorhinal cortex and hippocampus of patients with Alzheimer’s disease (Narisawa-Saito et al., 1996; Hock et al., 2000).”
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The Pleiotropic Potential of BDNF beyond Neurons: Implication for a Healthy Mind in a Healthy Body
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“…that BDNF gene therapy would serve as a preventive measure rather than as a radical treatment and that inducing the BDNF gene early would be helpful in preventing the reduction of BDNF expression levels observed in AD brains (Narisawa-Saito et al., 1996; Connor et al., 1997; Hock et al., 2000).”
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“, 2014) and is presumably caused by a loss of neurons (Narisawa-Saito et al., 1996).”
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“The NGF levels were determined by NGF enzyme immunoassay (EIA) as described previously (Narisawa-Saito et al., 1996).”
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“In AD, cortical and hippocampal production of NGF is not reduced (Crutcher et al., 1993; Scott et al., 1995; Fahnestock et al., 1996; Narisawa-Saito et al., 1996; Hellweg et al., 1998; Hock et al., 2000; Mufson et al., 2003b).”
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“…described above are conflicting but several studies describe a BDNF alteration at mRNA and protein level, in both the brain (Phillips et al., 1991; Narisawa-Saito et al., 1996) and the periphery (Laske et al., 2007; Angelucci et al., 2010), suggesting an involvement of this neurotrophin in AD.”
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“Human post mortem brain of AD Crutcher et al., 1993 Frontal cortex Occipital cortex Narisawa-Saito et al., 1996 Molor cortex Entorhinal cortex Dentate cortex Scott et al.,1995 Frontal, temporal, occipital cortex, hippocampus, amygdala, cerebellum, putamen Nucl.”
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Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production
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“…average level of BDNF compared to many other brain areas, including frontal, parietal, temporal and occipital cortices, putamen and thalamus (Durany et al. 2000; Karege et al. 2005), and up to 15 times the level of BDNF compared with the motor and entorhinal cortices (Narisawa-Saito et al. 1996).”
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Oroxylin A enhances memory consolidation through the brain-derived neurotrophic factor in mice
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Neuro-Immuno-Gene- and Genome-Editing-Therapy for Alzheimer’s Disease: Are We There Yet?
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A unifying hypothesis of Alzheimer's disease. II. Pathophysiological processes
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Soya phytoestrogens change cortical and hippocampal expression of BDNF mRNA in male rats
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“Narisawa-Saito et al. (1996) used the two-site immunoassays (EIAs) as a protein detection method.”
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Nanotechnology-based gene therapy as a credible tool in the treatment of Alzheimer’s disease
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“Narisawa-Saito et al., 1996 hAPP mice Lentiviral-based cathepsin B delivery Roles in neuroprotection and antiamyloidogenicity – Mueller-Steiner et al., 2006 Cathepsin B Aβ degradation Human wild-type APP (hAPPwt) mice Gene knockout Decreased Aβ40, Aβ42, and CTFβ by a large amount, which is…”
BackgroundTargeting brain‐derived neurotrophic factor in the treatment of neurodegenerative diseases: A review
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Plasma BDNF levels associate with Pittsburgh Compound B binding in the brain
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“Lower BDNF levels measured in brain [10–13], cerebrospinal fluid [14], and peripheral blood [5,15–19] are seen in subjects with AD and mild cognitive impairment (MCI) relative to controls.”
BackgroundRenin-Angiotensin System Alterations in the Human Alzheimer’s Disease Brain
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“Hampson et al. (1997) demonstrated that Cerebrolysin is able to increase the binding of BDNF to its receptor trkB.”
InfluentialBrain-derived neurotrophic factor in patients with frontotemporal dementia
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Lysosomal Dysfunction Reduces Brain-Derived Neurotrophic Factor Expression
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“NT-3 Neurotrophin-3 Motor cortex↓ [37]; no change in all brain regions [38]”
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“A decrease in BDNF protein levels in the entorhinal and temporal cortex of AD suffers has also been described [98].”
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“Post-mortem analysis shows reduced BDNF protein levels in brain regions affected by AD, indicating that a loss of neurotrophic support occurs in the disease along with other neuropathologies (Jiao et al. 2016; Lee et al. 2005; Narisawa-Saito et al. 1996).”
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Approach towards an integrative drug treatment of Alzheimer’s disease
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Targeting MicroRNAs Involved in the BDNF Signaling Impairment in Neurodegenerative Diseases
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“The expression of BDNF in the CNS is modified by numerous stimuli including physical exercise (Gomez- Pinilla et al. 2002; Ding et al. 2006; Garcia-Mesa et al. 2014), cognitive impairment (Buchman et al. 2016) and brain insults such as stress, seizure ischemia or hypoglycemic coma (Lindvall et al. 1994).”
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“For example, the amount of BDNF is reduced in the cortex and hippocampus of AD patients (Narisawa-Saito et al., 1996).”
Development of Precision Small-Molecule Proneurotrophic Therapies for Neurodegenerative Diseases
Janssens, J., Lu, D., Ni, B., Chadwick, W., Siddiqui, S., Azmi, A. S., Etienne, H., Jushaj, A., van Gastel, J., Martin, B., et al. (2016) · Vitamins and hormones · doi:10.1016/bs.vh.2016.10.006 · Cited by 8
Voigt, R. M., Raeisi, S., Yang, J., Leurgans, S. E., Forsyth, C. B., Buchman, A. S., Bennett, D. A., & Keshavarzian, A. (2021) · PLoS ONE · doi:10.1371/journal.pone.0240342 · Cited by 9
Brain-derived neurotrophic factor
Kakizawa, S. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-820649-2.00122-4 · Cited by 8
Beyin Kaynaklı Nörotrofik Faktör
Yarım, G. F., & Kazak, F. (2015) · Atatürk Üniversitesi Veteriner Bilimleri Dergisi · doi:10.17094/avbd.02290 · Cited by 8
“Alzheimer’lı hastaların ölümünden sonra beyin dokusunda azalmış BDNF mRNA ekspresyonu saptanmıştır (59,63).”
Hefti, F. F. (1999) · Handbook of experimental pharmacology · doi:10.1007/978-3-642-59920-0_7 · Cited by 8
Signals regulating neurotrophin expression in glial cells
Otten, U., März, P., Heese, K., Hock, C., Kunz, D., & Rose‐John, S. (2001) · Progress in brain research · doi:10.1016/s0079-6123(01)32102-7 · Cited by 8
Nagata, T., Shibata, N., Shinagawa, S., Nakayama, R., Kuerban, B., Ohnuma, T., Arai, H., Nakayama, K., & Yamada, H. (2013) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000354369 · Cited by 7
Age-modulated association between prefrontal NAA and the BDNF gene
Salehi, B., Preuss, N., van der Veen, J. W. C., Shen, J., Neumeister, A., Drevets, W. C., Hodgkinson, C. A., Goldman, D. A., Wendland, J. R., Singleton, A., et al. (2012) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145712001204 · Cited by 7
“Decreased expression of BDNF mRNA in the hippocampus has also been observed in Alzheimer’s patients (Connor et al., 1997; Narisawa-Saito et al., 1996; Phillips et al., 1991).”
BackgroundCunliffe, G., Lim, Y. T., Chae, W., & Jung, S. (2022) · Biomedicines · doi:10.3390/biomedicines10123064 · Cited by 6
Neuroprotective Strategies for Alzheimer’s Disease Prevention and Therapy
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Amyloid-Beta, BDNF, and the Mechanism of Neurodegeneration in Alzheimer’s Disease
Rosa, E., & Fahnestock, M. L. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_43 · Cited by 6
EPIGENETIC MECHANISMS IN ALZHEIMER'S DISEASE: STATE-OF-THE-ART
Faltraco, F., Lista, S., Garaci, F., & Hampel, H. (2012) · Cineca Institutional Research Information System (Tor Vergata University) · Cited by 5
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The role of brain-derived neurotrophic factor in neural circuit development and function
Autry, A. E., & Bambah-Mukku, D. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-823672-7.00020-x · Cited by 6
Romero‐Ramos, M., Venero, J. L., Santiago, M., et al. (2000) · Neuroscience · doi:10.1016/s0306-4522(00)00424-3 · Cited by 5
Shen, T., Sheriff, S., You, Y., Jiang, J., Schulz, A. M., Francis, H., Mirzaei, M., Saks, D., Palanivel, V., Basavarajappa, D. K., et al. (2024) · Aging and Disease · doi:10.14336/ad.2024.0346 · Cited by 5
“The BDNF levels in the entorhinal cortex were significantly lower in AD patients compared to healthy controls [70].”
BackgroundThe Pleiotropic Potential of BDNF beyond Neurons: Implication for a Healthy Mind in a Healthy Body
Rosa, M. C. D., Zimbone, S., Saab, M. W., & Tomasello, M. F. (2022) · Vide Leaf, Hyderabad eBooks · doi:10.37247/pabsc.1.22.35 · Cited by 3
NGF and BDNF Gene Therapy for Alzheimer’s Disease
Tuszynski, M. H., & Nagahara, A. H. (2016) · Springer eBooks · doi:10.1007/978-1-4899-7654-3_3 · Cited by 4
Zhang, J. C., Wang, J., Lin, J., Su, G., Shen, Y. L., Guo, Q., Cai, J. J., Liu, J. Y., Jia, K. X., & Fang, D. Z. (2023) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s412983 · Cited by 3
Metadata
- Authors
- Narisawa-Saito, M., Wakabayashi, K., Tsuji, S., Takahashi, H., & Nawa, H.
- Affiliations
- Brain Research Institute, Niigata University (JP)
- Venue
- NeuroReport
- Published
- 1996-11
- Volume
- 7
- Issue
- 18
- Pages
- 2925-2928
- ISSN
- 0959-4965 (ISSN-L)
- OpenAlex
- W2055746351
- Cited by
- 226
- References
- 0
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 6 · 2023: 6 · 2022: 7 · 2021: 10 · 2020: 11 · 2019: 5 · 2018: 6 · 2017: 6 · 2016: 12 · 2015: 6 · 2014: 9 · 2013: 15 · 2012: 10
- FWCI
- 3.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroreport (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, neurotrophins, nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, regional brain differences, dentate gyrus, entorhinal cortex, motor cortex
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Animals, Brain Chemistry, Humans, Immunoenzyme Techniques, Middle Aged, Nerve Growth Factors, Postmortem Changes, Rats, Sprague-Dawley, Entorhinal Cortex, Dentate Gyrus, Brain-Derived Neurotrophic Factor, Neurotrophin 3, Rats
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