Humanin 10mg

The core pathological features of AD include deposition of beta amyloid (A β) plaques and neurofibrillary tangles (NFTs), accompanied by neuronal loss and synaptic dysfunction. Neuroprotective agents may intervene in the AD process through multiple pathways, including:

Reduce A β production: Certain ingredients, such as curcumin and resveratrol, can inhibit the activity of β - secretase 1 (BACE1) and γ - secretase, reducing the production of toxic A β 42 fragments. For example, animal experiments have shown that curcumin treatment can reduce the level of A β 42 in the brain of APP/PS1 transgenic mice by 30%.

Promoting the clearance of A β: It may accelerate the clearance of A β in cerebrospinal fluid circulation by activating the phagocytic function of microglia (immune cells in the brain) or enhancing the permeability of the blood-brain barrier (BBB). For example, flavonoids in Ginkgo biloba extract can upregulate the expression of CD36 receptors in microglia and enhance A β phagocytic ability.
Protecting neurons: Antioxidant (clearing free radicals) and anti apoptotic (inhibiting caspase-3 activation) effects can delay neuronal death.

For example, neuroacids (a long-chain monounsaturated fatty acid) can stabilize neuronal membrane structure, reduce A β - induced calcium influx and mitochondrial damage.

Regulating neuroinflammation: AD patients have chronic neuroinflammation in their brains, and neuroprotective agents (such as omega-3 fatty acids) can protect neurons from inflammatory damage by inhibiting the NF - κ B signaling pathway and reducing the release of pro-inflammatory factors such as IL-1 β and TNF - α.

PD is characterized by degeneration and death of dopaminergic neurons in the substantia nigra, as well as the formation of Lewy bodies (α - synuclein aggregates). Possible protective mechanisms include:

Inhibition of alpha synuclein aggregation: Abnormal aggregation of alpha synuclein is a key pathological event in PD. Brain protective substances such as caffeine and EGCG may clear aggregates by stabilizing protein conformation or promoting autophagy lysosome pathways. For example, EGCG can bind to alpha synuclein, preventing its fibrosis formation.

Protecting mitochondrial function: The activity of mitochondrial complex I is reduced in PD patients, leading to oxidative stress and energy metabolism disorders.

The ergothionein (a natural antioxidant) in neuroprotective agents can be localized to mitochondria, directly clearing ROS and improving ATP synthesis. Animal experiments have shown that supplementation with ergotamine can improve the motor function of PD model mice by 40%.
Regulating dopamine metabolism: Brain protectants (such as mucilaginous frankincense acid) may alleviate PD symptoms by inhibiting monoamine oxidase (MAO-B) activity, reducing dopamine degradation.
Anti inflammatory effect: There is activation of microglia in the brain of PD patients, and neuroprotective agents (such as curcumin) can reduce the damage of neuroinflammation to dopaminergic neurons by inhibiting the activation of NLRP3 inflammasome.

MS is an autoimmune demyelinating disease characterized by central nervous system (CNS) white matter demyelination and axonal injury. Possible ways to intervene in the MS process include:

Promoting myelin regeneration: The neural acid component is an important component of myelin phospholipids, which can nourish oligodendrocyte precursor cells (OPCs), promote their differentiation into mature oligodendrocytes, and form new myelin sheaths. For example, nerve acid supplementation can increase the myelin regeneration rate by 50% in experimental autoimmune encephalomyelitis (EAE) mice.

Regulating immune response: Protecting it (such as vitamin D, omega-3 fatty acids) can alleviate damage to myelin sheaths from autoimmune attacks by inhibiting Th17 cell differentiation or promoting regulatory T cell (Treg) function.
Antioxidant protection: During the acute phase of MS, there is oxidative stress, and this substance (such as coenzyme Q10) can protect neurons and axons by enhancing antioxidant enzyme activity, reducing lipid peroxidation and DNA damage.

After cerebral ischemia, the sharp decrease in local cerebral blood flow (rCBF) leads to energy metabolism disorders and cell death. Possible mechanisms to improve cerebral perfusion include:

Dilation of cerebral blood vessels: Brain protective agents (such as Ginkgo biloba extract and Nimodipine) can activate potassium channels in vascular smooth muscle cells, causing vasodilation and increasing rCBF in ischemic areas. For example, terpenoids in Ginkgo biloba extract can significantly dilate cerebral arterioles, increasing rCBF by 25% -30%.

Reduce blood viscosity: Its (such as tanshinone) can inhibit platelet aggregation and red blood cell aggregation, reduce the risk of thrombosis, and thus improve cerebral microcirculation.
Anti delayed hypoperfusion: After cerebral ischemia-reperfusion, some patients may experience delayed neuronal necrosis (DND), which is associated with free radical bursts and inflammatory reactions during reperfusion. It (such as edaravone) can alleviate DND by clearing free radicals and inhibiting the release of inflammatory factors. Animal experiments have shown that edaravone can reduce the infarct volume by 40% in rats with cerebral ischemia.

After cerebral hemorrhage, edema, inflammatory reactions, and secondary brain damage may occur in the surrounding tissues of the hematoma. Possible ways to promote rehabilitation include:

Reduce brain edema: Its use (such as sodium aescinate) can alleviate brain edema by inhibiting vasogenic edema (reducing vascular permeability) and cytotoxic edema (stabilizing cell membranes). For example, sodium aescinate can reduce brain edema volume by 35% in rats with cerebral hemorrhage.
Promote hematoma absorption: Its (such as Xuefu Zhuyu Tang) may accelerate hematoma dissolution and absorption by activating the fibrinolytic system or enhancing macrophage phagocytic function.

Improving cerebral microcirculation: Its (such as rehabilitation tablets) can regulate vascular function, improve cerebral microcirculation status, and enhance blood-brain barrier protection by upregulating endothelial nitric oxide synthase (ecNOS) mRNA expression and downregulating endothelin-1 (ET-1) mRNA expression.
Promoting neural repair: Brain protective factors (such as nerve growth factor NGF) can stimulate axonal regeneration and synaptic remodeling, helping patients recover motor and cognitive functions.

Vascular dementia (VaD) is caused by repeated cerebral ischemia or hemorrhage, characterized by progressive decline in cognitive function. VaD may be prevented through the following mechanisms:

Anti atherosclerosis: brain protective factors (such as statins and phytosterols) can reduce the level of low-density lipoprotein cholesterol (LDL-C), inhibit the proliferation of vascular smooth muscle cells and the formation of foam cells, thereby reducing the risk of cerebrovascular events.
Improving cerebral blood flow: Brain protectants (such as vinblastine) can dilate cerebral blood vessels and inhibit platelet aggregation, increase cerebral perfusion, and improve brain tissue metabolism.

Protecting neurons: Brain protectants (such as phosphatidylcholine) can promote phospholipid synthesis and neurotransmitter release by providing choline and cytosine nucleotides, protecting neurons from ischemic damage.

HIE is a common brain injury in newborns, which may lead to sequelae such as epilepsy and cerebral palsy. Possible mechanisms to alleviate brain damage include:

Inhibition of calcium influx: During HIE, excessive activation of glutamate receptors leads to calcium influx, causing neuronal death. It (such as minocycline) can reduce calcium overload by inhibiting NMDA receptors or voltage-gated calcium channels.
Anti apoptotic effect: Melatonin, for example, can reduce neuronal apoptosis by inhibiting caspase-3 activation and Bax expression.

Animal experiments have shown that melatonin can reduce the infarct volume of HIE neonatal rats by 50%.

Anti inflammatory effect: There is an inflammatory response in the brain after HIE, and neuroprotective agents (such as irbesartan) can reduce the release of pro-inflammatory factors such as IL-6 and TNF - α by inhibiting the TLR4/NF - κ B pathway.
Promoting neural development: Its (such as neuroacids) can provide raw materials for myelin synthesis, promote oligodendrocyte differentiation, and improve long-term neural development outcomes.

As age increases, cognitive function gradually declines due to decreased cerebral blood flow, decreased metabolism, and increased oxidative stress. Possible mechanisms to maintain brain health in the elderly include:

Provide neuronutritional support: It (such as neuroacids, DHA) is an important component of neuronal membranes and myelin sheaths, which can promote synapse formation and neurotransmitter release, and maintain cognitive function. For example, DHA supplementation can increase memory test scores by 15% in older adults.
Improving cerebral microcirculation: Extracts such as Ginkgo biloba leaves and Vinpocetine can dilate cerebral blood vessels and inhibit platelet aggregation, increase cerebral perfusion, and improve brain tissue metabolism.

Antioxidant protection: Humanin 10mg (such as vitamin C and vitamin E) can eliminate free radicals, reduce lipid peroxidation and DNA damage, and protect neurons from age-related damage.
Regulating inflammation balance: Its compounds (such as curcumin and resveratrol) can reduce the risk of cognitive impairment by inhibiting the NF - κ B pathway, reducing chronic low-grade inflammation. For example, curcumin supplementation can reduce the level of inflammatory cytokine IL-6 in elderly people by 20%.
Protecting synaptic structure: Brain protectants (such as phospholipids) can stabilize synaptic membrane structure, reduce age-related synaptic loss, and maintain the efficiency of neural signal transduction. Animal experiments have shown that supplementation with phospholipids can increase synaptic density in elderly mice by 25%.