🚀 go-pugleaf

it's not a Beta-amyloid thing. the Beta-amyloid thing happens be-cause
'normal' transcription is prematurely interrupted be-cause 'latching' neural
dynamics are prematurely interrupted. for those who have AoK, it's a TD
E/I-minimization "ratchet-pawling" [Ap5] deficit.

the 'point' being that, researchers should look-elsewhere, a bit, starting
by looking =carefully= for 'abnormally'-high-frequency 'EEG'-type traces.
the sub-problem, here, is that the global EEG must be broken into
'component' sub-'parts' because the correlated 'abnormal' high-frequency
trace[s] will be masked within the global trace, as the nervous system
struggles to compensate with respect to the failing TD E/I-minimization
dynamics.

shouldn't be difficult to sort it out.

it's definitely =not= a Beta-amyloid thing.

the Beta-amyloid stuff occurs only as a by-product of the the failing TD
E/I-minimization dynamics. the Beta-amyloid is what 'congeals-out-of'
prematurely-interrupted transcription. [transcription that becomes
'supplanted' before it runs to completion.

it's curable, but the necessary cure is with respect to the TD
E/I-minimization deficit, not with respect to the Beta-amyloid stuff. fis
the TD E/I-minimization deficit, and, to the degree of such, the
Beta-amyloid abnormalities will go-away, and so will the symptomology.

Cheers, k. p. collins

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