Oral Microbiome and Cognitive Decline: Difference between revisions

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==Alzheimer's Disease Overview==
==Alzheimer's Disease Overview==
<br> Alzheimer's disease (AD) is the most common form of dementia, affecting millions of people worldwide and posing significant public health challenges <ref name=Ballard>[Ballard, Clive, Serge Gauthier, Anne Corbett, Carol Brayne, Dag Aarsland, and Emma Jones. “Alzheimer’s Disease.” The Lancet 377, no. 9770 (March 19, 2011): 1019–31. https://doi.org/10.1016/S0140-6736(10)61349-9.]</ref>. It is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired daily functioning <ref name=Scheltens>[Scheltens, Philip, et al. "Alzheimer's disease." The Lancet 388.10043 (2016): 505-517 https://doi.org/10.1016/S0140-6736(15)01124-1]</ref>. The exact cause of AD remains unclear, but it is believed to involve a complex interplay of genetic, environmental, and lifestyle factors (Querfurth and LaFerla 2010).
<br> Alzheimer's disease (AD) is the most common form of dementia, affecting millions of people worldwide and posing significant public health challenges <ref name=Ballard>[Ballard, Clive, Serge Gauthier, Anne Corbett, Carol Brayne, Dag Aarsland, and Emma Jones. “Alzheimer’s Disease.” The Lancet 377, no. 9770 (March 19, 2011): 1019–31. https://doi.org/10.1016/S0140-6736(10)61349-9.]</ref>. It is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired daily functioning <ref name=Scheltens>[Scheltens, Philip, et al. "Alzheimer's disease." The Lancet 388.10043 (2016): 505-517 https://doi.org/10.1016/S0140-6736(15)01124-1]</ref>. The exact cause of AD remains unclear, but it is believed to involve a complex interplay of genetic, environmental, and lifestyle factors <ref name=Querfurth>[Querfurth, Henry W., and Frank M. LaFerla. “Alzheimer’s Disease.” New England Journal of Medicine 362, no. 4 (January 28, 2010): 329–44. https://doi.org/10.1056/NEJMra0909142.]</ref>.
At the cellular level, two hallmark features of AD are the presence of extracellular amyloid plaques and intracellular neurofibrillary tangles (Scheltens et al. 2016). Amyloid plaques are primarily composed of aggregated amyloid-β (Aβ) peptides, which result from the cleavage of amyloid precursor protein (APP) by β- and γ-secretases (Querfurth and LaFerla 2010). The accumulation of Aβ peptides is thought to play a critical role in the pathogenesis of AD, although the exact mechanisms by which they contribute to neurodegeneration remain under investigation (Ballard et al. 2011).
At the cellular level, two hallmark features of AD are the presence of extracellular amyloid plaques and intracellular neurofibrillary tangles <ref name=Scheltens/>. Amyloid plaques are primarily composed of aggregated amyloid-β (Aβ) peptides, which result from the cleavage of amyloid precursor protein (APP) by β- and γ-secretases <ref name=Querfurth/>. The accumulation of Aβ peptides is thought to play a critical role in the pathogenesis of AD, although the exact mechanisms by which they contribute to neurodegeneration remain under investigation <ref name=Ballard/>.
Increasing evidence suggests that bacteria may play a role in the development of AD. One hypothesis is that certain bacterial infections, particularly those involving the oral cavity, can induce systemic inflammation and the production of pro-inflammatory cytokines, which may contribute to neuroinflammation and the accumulation of amyloid plaques (Querfurth and LaFerla 2010). In fact, some studies have identified specific oral pathogens, such as Porphyromonas gingivalis, in the brains of AD patients, supporting the potential link between oral microbiome dysbiosis and AD (Scheltens et al. 2016).
Increasing evidence suggests that bacteria may play a role in the development of AD. One hypothesis is that certain bacterial infections, particularly those involving the oral cavity, can induce systemic inflammation and the production of pro-inflammatory cytokines, which may contribute to neuroinflammation and the accumulation of amyloid plaques <ref name=Querfurth/>. In fact, some studies have identified specific oral pathogens, such as Porphyromonas gingivalis, in the brains of AD patients, supporting the potential link between oral microbiome dysbiosis and AD <ref name=Scheltens/>.
Given the significant public health burden of AD, understanding the potential role of bacteria and other factors in its pathogenesis is critical for developing effective prevention and treatment strategies (Ballard et al. 2011). Further research is needed to elucidate the complex interplay between the oral microbiome, systemic inflammation, and neurodegenerative processes in AD and other cognitive disorders. <br>
Given the significant public health burden of AD, understanding the potential role of bacteria and other factors in its pathogenesis is critical for developing effective prevention and treatment strategies <ref name=Ballard/>. Further research is needed to elucidate the complex interplay between the oral microbiome, systemic inflammation, and neurodegenerative processes in AD and other cognitive disorders. <br>


==Alzheimers Disease Overview==
==Alzheimers Disease Overview==

Revision as of 00:49, 17 April 2023

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Alzheimer's Disease Overview


Alzheimer's disease (AD) is the most common form of dementia, affecting millions of people worldwide and posing significant public health challenges [1]. It is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired daily functioning [2]. The exact cause of AD remains unclear, but it is believed to involve a complex interplay of genetic, environmental, and lifestyle factors [3]. At the cellular level, two hallmark features of AD are the presence of extracellular amyloid plaques and intracellular neurofibrillary tangles [2]. Amyloid plaques are primarily composed of aggregated amyloid-β (Aβ) peptides, which result from the cleavage of amyloid precursor protein (APP) by β- and γ-secretases [3]. The accumulation of Aβ peptides is thought to play a critical role in the pathogenesis of AD, although the exact mechanisms by which they contribute to neurodegeneration remain under investigation [1]. Increasing evidence suggests that bacteria may play a role in the development of AD. One hypothesis is that certain bacterial infections, particularly those involving the oral cavity, can induce systemic inflammation and the production of pro-inflammatory cytokines, which may contribute to neuroinflammation and the accumulation of amyloid plaques [3]. In fact, some studies have identified specific oral pathogens, such as Porphyromonas gingivalis, in the brains of AD patients, supporting the potential link between oral microbiome dysbiosis and AD [2]. Given the significant public health burden of AD, understanding the potential role of bacteria and other factors in its pathogenesis is critical for developing effective prevention and treatment strategies [1]. Further research is needed to elucidate the complex interplay between the oral microbiome, systemic inflammation, and neurodegenerative processes in AD and other cognitive disorders.

Alzheimers Disease Overview

Include some current research, with at least one figure showing data.

Section 3

Include some current research, with at least one figure showing data.

Section 4

Conclusion

References

  1. ↑ 1.0 1.1 1.2 [Ballard, Clive, Serge Gauthier, Anne Corbett, Carol Brayne, Dag Aarsland, and Emma Jones. “Alzheimer’s Disease.” The Lancet 377, no. 9770 (March 19, 2011): 1019–31. https://doi.org/10.1016/S0140-6736(10)61349-9.]
  2. ↑ 2.0 2.1 2.2 [Scheltens, Philip, et al. "Alzheimer's disease." The Lancet 388.10043 (2016): 505-517 https://doi.org/10.1016/S0140-6736(15)01124-1]
  3. ↑ 3.0 3.1 3.2 [Querfurth, Henry W., and Frank M. LaFerla. “Alzheimer’s Disease.” New England Journal of Medicine 362, no. 4 (January 28, 2010): 329–44. https://doi.org/10.1056/NEJMra0909142.]



Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2023, Kenyon College

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