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2. 3-Indolepropionic acid - Wikipedia

   en.wikipedia.org/wiki/3-indolepropionic_acid

   3-Indolepropionic acid (IPA), or indole-3-propionic acid, has been studied for its therapeutic value in the treatment of Alzheimer's disease.As of 2022 [3] IPA shows potential in the treatment of this disease, though the therapeutic effect of IPA depends on dose and time of therapy initiation.

3. Protein kinase A - Wikipedia

   en.wikipedia.org/wiki/Protein_kinase_A

   In cell biology, protein kinase A (PKA) is a family of serine-threonine kinase [1] whose activity is dependent on cellular levels of cyclic AMP (cAMP). PKA is also known as cAMP-dependent protein kinase (EC 2.7.11.11). PKA has several functions in the cell, including regulation of glycogen, sugar, and lipid metabolism.

4. Early long-term potentiation - Wikipedia

   en.wikipedia.org/wiki/Early_long-term_potentiation

   These findings [5] suggested that there is a PKA-dependent phase of LTP intermediate to E-LTP and L-LTP, which was called intermediate LTP (I-LTP). In the transgenic mice, on the other hand, LTP induced by two trains decayed faster than in wild-type mice, implying that excessive calcineurin activity suppresses both I-LTP and L-LTP.

5. Can antibiotics, vaccines, and antivirals help lower dementia ...

   www.aol.com/antibiotics-vaccines-antivirals-help...

   Dementia affects more than 55 million people worldwide at an estimated global cost of more than $1 trillion, and up to 70% of those people have Alzheimer’s disease.

6. HEPPS (buffer) - Wikipedia

   en.wikipedia.org/wiki/HEPPS_(buffer)

   HEPPS (EPPS) is a buffering agent used in biology and biochemistry.The pKa of HEPPS is 8.00. It is ones of Good's buffers. [1]Research on mice with Alzheimer's disease-like amyloid beta plaques has shown that HEPPS can cause the plaques to break up, reversing some of the symptoms in the mice.

7. Amyloid beta - Wikipedia

   en.wikipedia.org/wiki/Amyloid_beta

   Brain Aβ is elevated in people with sporadic Alzheimer's disease. Aβ is the main constituent of brain parenchymal and vascular amyloid; it contributes to cerebrovascular lesions and is neurotoxic. [ 33 ] [ 34 ] [ 35 ] It is unresolved how Aβ accumulates in the central nervous system and subsequently initiates the disease of cells.