Can you explain why? And how much smaller?

Yes - you have CD8 and CD4 T cells apart from the B cells that make antibodies. These adaptive immune cells routinely react to self-antigen and are then destroyed for doing so. Auto-immunity usually results from a failure of this filtering.

Usually in auto-immunity the CD4 cells coordinate a CD8 and B cell response to self-antigen, so the antibodies aren't super necessary. Theoretically, you could have an autoimmune reaction without self-reactive antibodies, but this would be uncommon.

Neutrophils are part of the innate immune system, which is rarely self reactive because its behaviour is genetically defined.

Bionic eyes are currently in development by the bionic ear team and they aren't that far away, although it'll probs start with simple shapes with poor resolution. But it's a simpler problem because you can interrogate the patient's optic nerve and augment stimuli to inform the way your device communicates.

On the other hand, transplants are much more challenging - the visual pathway from cone/rod passes through complex, multi-synapse neuronal processing. Neurons tend to degrade quickly and they aren't very good at repair. Then there's the rejection question. So you don't have a good way to figure out if you're connecting the right donor/patient neurons, and even if you did, they'd rapidly degrade.

Seems inefficient. Surely easier to transmit instructions for constructing the body and programming it to an existing intelligence. Which is like a mix between the plot of Contact and Species.

Yea, vibrant and enticing. Turns the everyday into something remarkable.

I used the term 'error bars' to describe the +/- values in the listed results. Frustratingly so far I haven't been able to access the original article in full text, so I can't be sure exactly what those 'error bars' represent. Presumably they're quoting the standard error in the samples, in which case, there appears to be a lot of error in their samples, which suggests that each estimate would have wide confidence intervals, which may overlap. Obviously overlapping confidence intervals don't necessarily mean that the difference isn't real, but if they overlap widely you'd certainly be quite skeptical of the results.

More specifically, let's look at some of the data in the abstract.

In the pre-treatment groups, the baseline BPND was 1.04 +/-0.31 vs 0.97 +/- 0.25. Is this a statistically significant difference? I don't know, but my guess would be that it isn't. Post exposure, the two groups' BPND was 0.87 +/- 0.24 vs 0.92 +/- 0.22. is this a statistically significant difference? Once again, I don't know, but my guess would be that it isn't.

If depressed people weren't measurably different from healthy controls in the baseline or post-treatment measures, then the fact that there is a within-group difference in the healthy controls but not in the depressed patients is much less convincing and seems more likely to be a statistical fluke.

Hijackingthe top comment for visibility. Copying comments from last time this was posted.

Probably could just ignore this result unless it's replicated.

"BPND was significantly reduced in the HC group (1.04±0.31 vs 0.87±0.24 , p < 0.001) but not in MDE (0.97 ± 0.25 vs 0.92 ± 0.22, ns)".

Those differences are apparently p-value significant, but the error bars overlap widely in each group.

In the absence of other opinions, I'll offer a perspective. In short, this is probably beyond the limits of our current understanding of neuroscience, but we have some guesses.

When people have lesions in the dominant temporal lobe they have trouble with recognising or linking the meanings of sounds and words. There is an equivalent semantic agnosis for some kinds of visual stimuli usually associated with lesions in the parietal lobe. In general, the brain tends to infer a pattern that explains disparate stimuli. The term for this is "gestalt". This is a high level function that is quite sensitive to lesional disruption - see The Man Who Mistook Hos Wife for a Hat for examples.

Semantic content in auditory stimuli, processed by the temporal lobe, is far more temporally dependent than other stimuli. Note that the term 'temporal' is shared between the lobe and the nature of it's processing is purely coincidental - it was named for the tendency of the hair of the overlying scalp to gray, showing age, before other areas of hair.

In any case, when the temporal lobe receives a segment of data that activates a specific semantic 'gestalt', it likely continues to seek confirmation of that 'gestalt'. For smells or tactile senses, or visual stimuli, it's simpler, because you just sniff or feel more, or double take. For songs, the new stimuli only adds to the gestalt if it occurs in a specific temporal sequence. As such, you need to continue the tune, either in your head, by humming, or listening to the song.

Edit: Source - I'm a neuropsychiatry registrar in an epilepsy unit, and I've read the first few chapters of Lishman's?