Role of ketogenic diet in neurodegenerative diseases focusing on Alzheimer diseases: The guardian angle
The ketogenic diet (KD) is a low-carbohydrate, adequate protein and high-fat diet. KD is primarily used to treat refractory epilepsy. KD was shown to be effective in treating different neurodegenerative diseases. Alzheimer disease (AD) is the first common neurodegenerative disease in the world chara...
Saved in:
Published in | Ageing research reviews Vol. 95; p. 102233 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier B.V
01.03.2024
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | The ketogenic diet (KD) is a low-carbohydrate, adequate protein and high-fat diet. KD is primarily used to treat refractory epilepsy. KD was shown to be effective in treating different neurodegenerative diseases. Alzheimer disease (AD) is the first common neurodegenerative disease in the world characterized by memory and cognitive impairment. However, the underlying mechanism of KD in controlling of AD and other neurodegenerative diseases are not discussed widely. Therefore, this review aims to revise the fundamental mechanism of KD in different neurodegenerative diseases focusing on the AD. KD induces a fasting-like which modulates the central and peripheral metabolism by regulating mitochondrial dysfunction, oxidative stress, inflammation, gut-flora, and autophagy in different neurodegenerative diseases. Different studies highlighted that KD improves AD neuropathology by regulating synaptic neurotransmission and inhibiting of neuroinflammation and oxidative stress. In conclusion, KD improves cognitive function and attenuates the progression of AD neuropathology by reducing oxidative stress, mitochondrial dysfunction, and enhancing neuronal autophagy and brain BDNF.
•KD is a low carbohydrate and high fat diet activates neuronal autophagy, brain BDNF, and can attenuate AD neuropathology.•KD improves cognitive function.•KD attenuates the progression of AD neuropathology by reducing oxidative stress, mitochondrial dysfunction. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 1568-1637 1872-9649 1872-9649 |
DOI: | 10.1016/j.arr.2024.102233 |