Population ageing has increased dramatically worldwide and the proportion of adults aged 60 and over is expected to reach 22% by 2050. [1]
CONTENTS
- Alzheimer’s disease, a cognitive disorder with as yet unknown causes
- Microglia activation, a double-edged sword
- NMN counters Alzheimer’s disease
Alzheimer’s disease, a cognitive disorder with as yet unknown causes
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a gradual decline in memory and cognitive ability [2]. Amyloid plaques (A β ) formed by extracellular deposition are the main pathological feature. However, the cause of BA is complex and not yet fully understood. Currently, there is no effective treatment for this condition. Clinical treatment drugs for BA are mainly to improve symptoms and attenuate progression, such as cholinesterase inhibitors. It is the most common progressive neurodegenerative disease, and the gut flora and its metabolites play an important role in alleviating central nervous system disorders.
Microglial cell activation, a double-edged sword
As immune cells in the central nervous system, microglial cells play a key role in brain development and in building immunity and can also eliminate the deposition of amyloid β (A β) [3]. Under normal physiological conditions, these cells regulate the microenvironment to maintain the brain’s ability to maintain its various physiological constants. Under conditions of abnormal stress, microglial cells can rapidly expand their cellular processes, go to the injured site, remove noxious substances and induce an immune response by releasing inflammatory factor. Microglia account for about 10% of all cells in the nervous system. Microglial overactivation is a hallmark of brain ageing and coincides with age-related neurodegeneration and cognitive decline. Microglial activation is closely linked to the deposition of amyloid plaques. Detection of Aβ peptide by microglia leads to the removal of Aβ peptide and other harmful substances. However, microglia action and senile plaque deposition is a double-edged sword. Although microglia are useful in sensing the brain environment, the continued production of amyloid plaque deposits and chronic interaction with microglia may reduce the ability of microglia to remove amyloid deposits and lead to phagocytic dysfunction, exacerbating AD damage.
[4]
NMN counters Alzheimer’s disease
According to these studies, NMN fights Alzheimer’s disease by activating autophagy – the consumption of one’s own tissues by an organism undergoing starvation – and antioxidant stress. Nicotinamide mononucleotide (NMN), one of the precursors for the synthesis of nicotinamide adenine dinucleotide (NAD+), reduces the brain features of AD, including neuroinflammation, mitochondrial abnormalities, synaptic dysfunction and cognitive impairment. [5]
SURSE [1] – The 2024 Revision of World Population Prospects [2] – Specks of insight into Alzheimer’s disease [3] – Mechanisms of Amyloid-β Peptide Clearance: Potential Therapeutic Targets for Alzheimer’s Disease [4] – Aβ promotes CD38 expression in senescent microglia in Alzheimer’s disease [5] – Nicotinamide mononucleotide improves the Alzheimer’s disease by regulating intestinal microbiota