When Encephalitis Injures the Brain: Neuroprotection, BDNF, and the Science of Brain Resilience.
Executive Brief
Neuroprotection, BDNF & Brain
Resilience in Encephalitis:
Scientific Context for KESUM® (Persicaria
minor) & PHYSTA®**
1. Clinical Context: Encephalitis
& Brain Injury
Nipah virus infection is
frequently complicated by acute encephalitis, a condition associated with high
mortality & long-term neurological disability.
Neuroimaging findings report:
·
Hyperintense MRI lesions in ~71% of cases
·
Predominant involvement of the temporal lobes &
pons
·
Bilateral white-matter abnormalities
Pathophysiology consistent with
micro-embolic injury, neuroinflammation & cerebral edema
These changes reflect structural &
functional brain injury, not merely transient inflammation, & are strongly
associated with impaired cognitive recovery among survivors.
2. Why BDNF Matters in
Encephalitis
Brain-Derived Neurotrophic Factor
(BDNF) is a central regulator of:
·
Neuronal survival under inflammatory stress
·
Synaptic plasticity & reconnection
·
White-matter integrity
·
Cognitive & psychosocial recovery
Clinical neuroscience literature
consistently shows that declining BDNF levels correlate with worse neurological
outcomes, including persistent cognitive impairment after encephalitis, stroke
& neurodegenerative conditions.
In severe brain inflammation,
preserving neurotrophic capacity becomes a critical determinant of recovery.
3. Human Clinical Evidence:
Polygonum minus (KESUM® / Biokesum®)
A randomized, double-blind,
placebo-controlled human trial evaluated the effects of Polygonum minus extract
over 6 months.
Key clinically significant
findings:
·
BDNF increased by 2.03% in the Biokesum® group
·
BDNF decreased by 19.19% in the placebo group (p
< 0.05)
·
Triglycerides reduced by 19.05% in the Biokesum®
group, while increasing in placebo
The significance lies not only in
BDNF elevation, but in prevention of BDNF decline, a factor strongly linked to
neuronal vulnerability under inflammatory stress.
These findings support the role
of KESUM® as a neuroprotective & neuro-resilience -supporting botanical,
rather than a disease-curative agent.
4. Relevance to Brain Swelling
& Hyperintense Lesions
Hyperintense MRI lesions
represent:
·
Axonal stress
·
Microvascular injury
·
Disrupted neural connectivity
BDNF-supported pathways are
directly involved in:
·
Neuronal survival signaling
·
Repair of synaptic connections
Functional recovery following
inflammatory or ischemic injury
Thus, maintenance of BDNF may
influence the brain’s ability to withstand & recover from encephalitic
damage, including white-matter injury associated with edema &
micro-embolism.
5. Complementary Role of PHYSTA®
(Tongkat Ali)
Across 26 published clinical
studies (14 conducted by Biotropics), PHYSTA® has demonstrated:
·
Stress & cortisol modulation
·
Energy metabolism support
·
Immune & physiological resilience
In the context of severe
infections:
·
Systemic stress & metabolic exhaustion
exacerbate neuroinflammation
·
Physiological resilience indirectly supports
neurological outcomes
PHYSTA® is therefore best
positioned as systemic resilience support, complementary to neurotrophic
strategies.
6. Integrated - Scientific.
Encephalitis damages the brain
structurally.
BDNF determines recovery
capacity.
KESUM® supports neurotrophic
resilience.
PHYSTA® supports systemic stress
adaptation.
This framework aligns with
current neuroscience understanding while remaining ethically, clinically &
regulatorily sound.
7. Nipah virus - related
encephalitis results in significant inflammatory & microvascular brain
injury.
Neurological outcomes depend not
only on infection control, but on preservation of intrinsic brain repair
mechanisms.
Human clinical evidence supports
Polygonum minus (KESUM®) in maintaining & modestly enhancing BDNF, a key
factor in brain resilience.
PHYSTA® supports systemic stress
response & immune balance.
Both should be positioned as
supportive, not therapeutic, interventions for brain & systemic resilience.
Scientific - Statement :
“In severe encephalitic stress,
preserving neurotrophic capacity & systemic resilience may influence
neurological outcomes beyond infection control alone.”
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